bec-1

UniProt ID: Q22592
Organism: Caenorhabditis elegans
Review Status: COMPLETE
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Gene Description

BEC-1 is the C. elegans ortholog of yeast Atg6/Vps30 and mammalian Beclin-1, functioning as an essential scaffold/adaptor subunit of the class III phosphatidylinositol 3-kinase (PI3K) complex. BEC-1 assembles with VPS-34 (the catalytic PI3K subunit) and VPS-15 to form complexes that generate phosphatidylinositol 3-phosphate (PtdIns3P) on membranes. In the PI3KC3-C1 complex (with EPG-8/ATG14), BEC-1 promotes autophagosome nucleation at ER-derived omegasomes. In the PI3KC3-C2 complex (with UVRAG/VPS-38), BEC-1 supports endocytic trafficking, endosome-to-Golgi retrograde transport, and phagosome maturation. BEC-1 also interacts with CED-9 (BCL-2 family) to negatively regulate apoptosis. The protein is essential for dauer morphogenesis, lifespan extension in insulin signaling mutants, survival during starvation, clearance of apoptotic corpses, germline stem cell proliferation, and protection against protein aggregation toxicity.

Existing Annotations Review

GO Term Evidence Action Reason
GO:0000045 autophagosome assembly
IBA
GO_REF:0000033 		ACCEPT
Summary: BEC-1 is a core component of the PI3KC3-C1 complex that initiates autophagosome formation. Evidence from PMID:12958363 demonstrates that bec-1 is essential for autophagosome formation in seam cells during dauer development. BEC-1 functions with VPS-34 to generate PtdIns3P at phagophore assembly sites, which is required for recruitment of downstream autophagy machinery including LGG-1/LC3.
Reason: This is a core molecular function of BEC-1 as the Beclin ortholog. Multiple studies confirm BEC-1's essential role in autophagosome assembly as part of the PI3KC3 complex.
Supporting Evidence:
PMID:12958363
bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension
PMID:16111945
We demonstrate that BEC-1 is necessary for the function of the class III PI3 kinase LET-512/Vps34, an essential protein required for autophagy
GO:0000423 mitophagy
IBA
GO_REF:0000033 		ACCEPT
Summary: Mitophagy is a selective form of autophagy that degrades mitochondria. While BEC-1 is essential for general autophagy, there is limited direct experimental evidence specifically demonstrating BEC-1's role in mitophagy in C. elegans. The IBA annotation is based on phylogenetic inference from mammalian Beclin-1.
Reason: As a core component of the autophagy initiation complex, BEC-1 would be required for mitophagy, which is a selective form of macroautophagy. The phylogenetic inference is sound given the conserved role of Beclin/Atg6 proteins in all forms of autophagy.
Supporting Evidence:
file:worm/bec-1/bec-1-deep-research-falcon.md
BEC-1 functions primarily as a scaffold/adaptor for class III PI3K complexes (VPS-34 with VPS-15) that assemble with complex-specific partners
GO:0030674 protein-macromolecule adaptor activity
IBA
GO_REF:0000033 		ACCEPT
Summary: BEC-1 functions as a scaffold/adaptor within the PI3KC3 complex, bridging VPS-34 (the catalytic kinase) with other complex components (EPG-8/ATG14, UVRAG) and regulatory proteins (CED-9, SORF-1, SORF-2). BEC-1 does not have enzymatic activity itself but positions VPS-34 to generate PtdIns3P at appropriate membrane sites.
Reason: This accurately describes BEC-1's primary molecular function. BEC-1 serves as an adaptor between the VPS-34 kinase and other complex components, consistent with the Beclin family's role across eukaryotes.
Supporting Evidence:
PMID:16111945
Furthermore, BEC-1 forms a complex with the antiapoptotic protein CED-9/Bcl-2
PMID:21116129
EPG-8 directly interacts with the C. elegans Beclin 1 homolog, BEC-1
GO:0043548 phosphatidylinositol 3-kinase binding
IBA
GO_REF:0000033 		ACCEPT
Summary: BEC-1 directly binds VPS-34, the class III PI3K catalytic subunit, forming the core of the PI3KC3 complex. This interaction is essential for VPS-34 function in both autophagy and endocytic trafficking.
Reason: Direct experimental evidence from C. elegans confirms BEC-1 binds VPS-34. This is a fundamental aspect of BEC-1 molecular function.
Supporting Evidence:
PMID:16111945
We demonstrate that BEC-1 is necessary for the function of the class III PI3 kinase LET-512/Vps34
file:worm/bec-1/bec-1-uniprot.txt
Interacts with vps-34 (PubMed:16111945, PubMed:26783301)
GO:0034271 phosphatidylinositol 3-kinase complex, class III, type I
IBA
GO_REF:0000033 		ACCEPT
Summary: The class III PI3K complex type I (PI3KC3-C1) contains VPS-34, VPS-15, Beclin, and ATG14 and functions specifically in autophagy initiation. In C. elegans, BEC-1 interacts with EPG-8 (the ATG14 homolog) for autophagy-specific functions.
Reason: BEC-1 is confirmed to be part of the autophagy-specific PI3KC3 complex containing EPG-8/ATG14. The interaction between BEC-1 and EPG-8 has been experimentally demonstrated.
Supporting Evidence:
PMID:21116129
EPG-8 directly interacts with the C. elegans Beclin 1 homolog, BEC-1. Our study demonstrates that epg-8 may function as a highly divergent homolog of the yeast autophagy gene Atg14
GO:0034272 phosphatidylinositol 3-kinase complex, class III, type II
IBA
GO_REF:0000033 		ACCEPT
Summary: The class III PI3K complex type II (PI3KC3-C2) contains VPS-34, VPS-15, Beclin, and UVRAG and functions in endocytic trafficking. BEC-1 has documented roles in endocytic retrograde transport and endosome maturation consistent with PI3KC3-C2 function.
Reason: BEC-1's role in endocytic trafficking is well documented. Evidence shows BEC-1 functions in the endosome-specific PI3KC3-C2 complex.
Supporting Evidence:
PMID:21183797
BEC-1, the C. elegans ortholog of Atg6/Vps30/Beclin1, a key regulator of the autophagic machinery, also contributes to endosome function
file:worm/bec-1/bec-1-deep-research-falcon.md
In PI3KC3-C2 (VPS-34-VPS-15-VPS-38/UVRAG-BEC-1), it supports endocytic/phagosomal maturation and endolysosomal trafficking
GO:0000407 phagophore assembly site
IBA
GO_REF:0000033 		ACCEPT
Summary: BEC-1 localizes to sites of autophagosome initiation (phagophore assembly sites/PAS) where it functions with VPS-34 to generate PtdIns3P required for autophagy initiation. The deep research indicates BEC-1 is recruited to ER/omegasome-phagophore sites.
Reason: As an essential component of the autophagy initiation PI3KC3-C1 complex, BEC-1 must localize to phagophore assembly sites. This is consistent with its role in autophagosome nucleation.
Supporting Evidence:
file:worm/bec-1/bec-1-deep-research-falcon.md
BEC-1 localizes to ER-associated omegasomes/phagophores during autophagy initiation, to autophagosomes, and to single-membrane phagosomes during LAP
GO:0006995 cellular response to nitrogen starvation
IBA
GO_REF:0000033 		KEEP AS NON CORE
Summary: Autophagy is induced under nitrogen starvation conditions. While general starvation response has been documented for bec-1, specific nitrogen starvation response in C. elegans has not been directly demonstrated. The annotation is based on phylogenetic inference.
Reason: While BEC-1 is clearly required for starvation survival (PMID:17785524), the specific nitrogen starvation response is inferred rather than directly demonstrated in C. elegans. Keep as non-core since the broader starvation response annotation is more directly supported.
Supporting Evidence:
PMID:17785524
Here we show that physiological levels of autophagy act to promote survival in Caenorhabditis elegans during starvation
GO:0045324 late endosome to vacuole transport
IBA
GO_REF:0000033 		ACCEPT
Summary: BEC-1 functions in endosomal trafficking including the conversion of early to late endosomes and subsequent transport. The PI3KC3 complex generates PtdIns3P required for endosome maturation and transport.
Reason: BEC-1's role in endosomal transport is well documented. Evidence from PMID:26783301 shows BEC-1 is required for proper early-to-late endosome conversion and transport.
Supporting Evidence:
PMID:21183797
we report that BEC-1, the C. elegans ortholog of Atg6/Vps30/Beclin1, a key regulator of the autophagic machinery, also contributes to endosome function
GO:0005737 cytoplasm
IEA
GO_REF:0000044 		ACCEPT
Summary: BEC-1 is localized to the cytoplasm. This is consistent with direct experimental evidence from PMID:16111945.
Reason: IDA evidence from PMID:16111945 confirms cytoplasmic localization. The IEA annotation is redundant but correct.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
SUBCELLULAR LOCATION: Cytoplasm {ECO:0000269|PubMed:16111945}
GO:0005768 endosome
IEA
GO_REF:0000044 		ACCEPT
Summary: BEC-1 localizes to endosomes where it functions as part of the PI3KC3-C2 complex in endocytic trafficking. Evidence from PMID:21183797 shows endosomal localization.
Reason: UniProt annotation based on experimental evidence from PMID:21183797 confirms endosomal localization.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
Endosome {ECO:0000269|PubMed:21183797}. Note=Co-localizes with rme-8, a component of the retromer complex, on endosomes
GO:0006897 endocytosis
IEA
GO_REF:0000043 		ACCEPT
Summary: BEC-1 is required for proper endocytosis and endosome function. Loss of bec-1 impairs fluid phase endocytosis and endosome-to-Golgi retrograde transport.
Reason: Multiple studies confirm BEC-1's role in endocytosis. This is a well-established function of Beclin/Atg6 proteins.
Supporting Evidence:
PMID:16111945
We demonstrate that BEC-1 is necessary for the function of the class III PI3 kinase LET-512/Vps34, an essential protein required for autophagy, membrane trafficking, and endocytosis
GO:0006914 autophagy
IEA
GO_REF:0000120 		ACCEPT
Summary: BEC-1 is essential for autophagy. This is the core function of Beclin/Atg6 family proteins across eukaryotes.
Reason: Autophagy is the primary biological process for which BEC-1 is required. This is supported by extensive experimental evidence.
Supporting Evidence:
PMID:12958363
bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension
GO:0030424 axon
IEA
GO_REF:0000044 		ACCEPT
Summary: BEC-1 is expressed in neurons including axonal regions. Expression in ventral nerve cord and nerve ring has been documented.
Reason: UniProt subcellular location annotation based on experimental evidence showing BEC-1 expression in neurons.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
Cell projection, axon {ECO:0000269|PubMed:17327275}
GO:0030425 dendrite
IEA
GO_REF:0000044 		ACCEPT
Summary: BEC-1 is expressed in neuronal cells including dendrites based on UniProt subcellular location annotation.
Reason: UniProt annotation based on experimental evidence of neuronal expression.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
Cell projection, dendrite {ECO:0000269|PubMed:17327275}
GO:0043204 perikaryon
IEA
GO_REF:0000044 		ACCEPT
Summary: BEC-1 is localized to neuronal cell bodies (perikarya) based on expression in neurons.
Reason: UniProt annotation supported by evidence of neuronal expression.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
Perikaryon {ECO:0000269|PubMed:17327275}
GO:0005515 protein binding
IPI
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate leve... 		MODIFY
Summary: BEC-1 binds to SORF-1 and SORF-2, which regulate PI3KC3 complex activity. The interaction was demonstrated by co-immunoprecipitation and pull-down assays.
Reason: The term 'protein binding' is too vague. BEC-1 specifically functions as an adaptor within the PI3KC3 complex. The interaction with SORF-1/2 is regulatory and should be captured by the adaptor activity annotation.
Supporting Evidence:
PMID:26783301
SORF-1 and SORF-2 act in a complex with BEC-1/Beclin1
GO:0036093 germ cell proliferation
IMP
PMID:28285998
A Non-Cell-Autonomous Role of BEC-1/BECN1/Beclin1 in Coordin... 		KEEP AS NON CORE
Summary: BEC-1 is required for germline stem cell proliferation during late larval and adult stages. RNAi knockdown of bec-1 reduces stem cell proliferation in the germline.
Reason: This is a documented phenotype of bec-1 loss but represents a pleiotropic developmental role rather than the core molecular function. The study shows this is non-cell-autonomous.
Supporting Evidence:
PMID:28285998
We found that autophagy genes such as bec-1/BECN1/Beclin1, atg-16.2/ATG16L, atg-18/WIPI1/2, and atg-7/ATG7 are required for the late larval expansion of germline stem cell progenitors
GO:0042078 germ-line stem cell division
IMP
PMID:28285998
A Non-Cell-Autonomous Role of BEC-1/BECN1/Beclin1 in Coordin... 		KEEP AS NON CORE
Summary: BEC-1 promotes cell-cycle progression and stem cell division in the germline during development.
Reason: This is a developmental phenotype reflecting BEC-1's role in cellular homeostasis rather than its core molecular function.
Supporting Evidence:
PMID:28285998
we report that BEC-1/BECN1/Beclin1 functions non-cell-autonomously to facilitate cell-cycle progression and stem cell proliferation
GO:0048284 organelle fusion
IMP
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate leve... 		MODIFY
Summary: BEC-1 is required for endosome fusion. Loss of bec-1 in combination with SORF genes affects early endosome fusion events.
Reason: The term is too general. The evidence specifically supports a role in endosome fusion/maturation, not organelle fusion broadly.
Supporting Evidence:
PMID:26783301
Loss of sorf-1 or sorf-2 leads to greatly elevated endosomal PtdIns3P, which drives excessive fusion of early endosomes
PMID:21183797
The Atg6/Vps30/Beclin 1 ortholog BEC-1 mediates endocytic retrograde transport in addition to autophagy in C.
GO:0048284 organelle fusion
IGI
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate leve... 		MODIFY
Summary: IGI evidence for organelle fusion based on genetic interactions with SORF-1, SORF-2, and VPS-34.
Reason: Same as above - term is too general for the specific endosomal fusion role supported by the evidence.
Supporting Evidence:
PMID:26783301
sorf-1 and sorf-2 function coordinately with Rab switching genes to inhibit synthesis of PtdIns3P, allowing its turnover for endosome conversion
GO:0051036 regulation of endosome size
IGI
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate leve... 		ACCEPT
Summary: BEC-1 affects endosome size through its role in generating PtdIns3P via the PI3KC3 complex. Genetic interactions with SORF-1/2 modulate endosome size.
Reason: This is well supported by evidence from PMID:26783301 showing that BEC-1 and SORF proteins regulate PtdIns3P levels which controls endosome size and fusion.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
Double knockout with either sorf-1 or sorf-2 results in smaller endosomes and an irregular distribution pattern of PtdIns3P in the cytoplasm (PubMed:26783301)
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate levels in early-to-late endosome conversion.
GO:2000643 positive regulation of early endosome to late endosome transport
IGI
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate leve... 		ACCEPT
Summary: BEC-1 positively regulates early-to-late endosome conversion through generating PtdIns3P required for endosome maturation.
Reason: Evidence clearly supports BEC-1's role in early-to-late endosome conversion through PtdIns3P generation.
Supporting Evidence:
PMID:26783301
These findings reveal a conserved mechanism that controls appropriate PtdIns3P levels in early-to-late endosome conversion
GO:0045138 nematode male tail tip morphogenesis
IMP
PMID:17890369
Autophagy genes unc-51 and bec-1 are required for normal cel... 		KEEP AS NON CORE
Summary: bec-1 mutants show defects in male tail ray pattern formation, indicating a role in developmental morphogenesis.
Reason: This is a developmental phenotype that likely reflects BEC-1's general role in autophagy/cellular homeostasis rather than a specific function in male tail morphogenesis.
Supporting Evidence:
PMID:17890369
mutational inactivation of two autophagy genes unc-51/atg1 and bec-1/atg6/beclin1 results in small body size without affecting cell number
GO:0008340 determination of adult lifespan
IGI
PMID:21906946
Autophagy and lipid metabolism coordinately modulate life sp... 		ACCEPT
Summary: bec-1 is required for lifespan extension in germline-less animals. Autophagy and lipid metabolism coordinately modulate lifespan and both require bec-1.
Reason: BEC-1-dependent autophagy is required for multiple longevity pathways including insulin signaling mutants, dietary restriction, and germline-less animals. This is a well-documented phenotype.
Supporting Evidence:
PMID:21906946
Germline removal extends life span in C. elegans via genes such as the lipase LIPL-4; however, less is known of the cellular basis for this life-span extension
GO:0043277 apoptotic cell clearance
IMP
PMID:21183797
The Atg6/Vps30/Beclin 1 ortholog BEC-1 mediates endocytic re... 		ACCEPT
Summary: BEC-1 is required for clearance of apoptotic cell corpses in the gonad, likely through its role in phagosome maturation.
Reason: The evidence directly supports BEC-1's role in apoptotic cell clearance through phagosome maturation. This represents a non-canonical function of BEC-1 in single-membrane processing.
Supporting Evidence:
PMID:21183797
We further identify a requirement for BEC-1 in the clearance of apoptotic corpses in the hermaphrodite gonad, suggesting a role for BEC-1 in phagosome maturation
GO:0005515 protein binding
IPI
PMID:21116129
The coiled-coil domain protein EPG-8 plays an essential role... 		MODIFY
Summary: BEC-1 directly interacts with EPG-8 (ATG14 homolog), which is required for autophagy function.
Reason: Protein binding is too vague. This interaction is part of BEC-1's adaptor function within the PI3KC3-C1 complex.
Supporting Evidence:
PMID:21116129
EPG-8 directly interacts with the C. elegans Beclin 1 homolog, BEC-1
GO:0008340 determination of adult lifespan
IGI
PMID:17912023
Autophagy is required for dietary restriction-mediated life ... 		ACCEPT
Summary: bec-1 is required for dietary restriction-mediated lifespan extension in eat-2 mutants.
Reason: Well-documented role of bec-1 in autophagy-dependent lifespan extension.
Supporting Evidence:
PMID:17912023
two essential autophagy genes (bec-1 and Ce-atg7) are required for the longevity phenotype of the C. elegans dietary restriction mutant
GO:0009267 cellular response to starvation
IMP
PMID:17785524
Dual roles of autophagy in the survival of Caenorhabditis el... 		ACCEPT
Summary: BEC-1-dependent autophagy is induced during starvation and promotes survival. Physiological levels of autophagy are required for starvation survival.
Reason: Clear experimental evidence that bec-1-dependent autophagy is required for starvation survival in C. elegans.
Supporting Evidence:
PMID:17785524
we show that physiological levels of autophagy act to promote survival in Caenorhabditis elegans during starvation
GO:0040014 regulation of multicellular organism growth
IGI
PMID:17890369
Autophagy genes unc-51 and bec-1 are required for normal cel... 		KEEP AS NON CORE
Summary: bec-1 mutants affect body size. Loss-of-function mutations in unc-51 and bec-1 suppress the giant phenotype of insulin/IGF-1 and TGF-beta signaling mutants.
Reason: This reflects BEC-1's role in cellular homeostasis affecting organism growth, rather than a direct regulatory function.
Supporting Evidence:
PMID:17890369
mutational inactivation of two autophagy genes unc-51/atg1 and bec-1/atg6/beclin1 results in small body size without affecting cell number
GO:0030163 protein catabolic process
IMP
PMID:17172799
Autophagy genes protect against disease caused by polyglutam... 		ACCEPT
Summary: BEC-1-dependent autophagy promotes clearance of polyglutamine protein aggregates. Inactivation of autophagy genes accelerates accumulation of polyQ aggregates.
Reason: Autophagy-dependent protein degradation is a core function of BEC-1. Clear evidence for role in polyQ aggregate clearance.
Supporting Evidence:
PMID:17172799
genetic inactivation of autophagy genes accelerates the accumulation of polyQ40 aggregates in C. elegans muscle cells
GO:0012501 programmed cell death
IGI
PMID:17327275
Influence of autophagy genes on ion-channel-dependent neuron... 		ACCEPT
Summary: bec-1 modulates necrotic cell death in neurons with hyperactive ion channels. Inactivation of bec-1 partially suppresses degeneration of neurons with toxic ion channel variants.
Reason: Evidence shows bec-1 contributes to necrotic cell death in specific contexts. Also, BEC-1 interacts with CED-9 to regulate apoptosis.
Supporting Evidence:
PMID:17327275
Inactivation of unc-51, bec-1 and lgg-1, the worm counterparts of the yeast autophagy genes Atg1, Atg6 and Atg8 respectively, partially suppresses degeneration of neurons with toxic ion channel variants
PMID:16111945
BEC-1 forms a complex with the antiapoptotic protein CED-9/Bcl-2, and its depletion triggers CED-3/Caspase-dependent PCD
GO:0005634 nucleus
IDA
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic ... 		ACCEPT
Summary: BEC-1 was detected in the nucleus by direct experimental observation. This may represent a regulatory or signaling role.
Reason: Direct experimental evidence (IDA) from PMID:16111945.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
IDA:WormBase. Cytoplasm. Nucleus. Cytoplasmic vesicle
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic cell death in C.
GO:0005737 cytoplasm
IDA
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic ... 		ACCEPT
Summary: BEC-1 is localized to the cytoplasm where it functions in autophagy and endosomal trafficking.
Reason: Direct experimental evidence (IDA) from PMID:16111945.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
SUBCELLULAR LOCATION: Cytoplasm {ECO:0000269|PubMed:16111945}
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic cell death in C.
GO:0031410 cytoplasmic vesicle
IDA
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic ... 		ACCEPT
Summary: BEC-1 localizes to cytoplasmic vesicles including autophagosomes and endosomes.
Reason: Direct experimental evidence (IDA) consistent with BEC-1's function at autophagosomal and endosomal membranes.
Supporting Evidence:
file:worm/bec-1/bec-1-uniprot.txt
GO:0031410; C:cytoplasmic vesicle; IDA:WormBase
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic cell death in C.
GO:0006914 autophagy
IGI
PMID:12958363
Autophagy genes are essential for dauer development and life... 		ACCEPT
Summary: bec-1 is required for autophagy, as demonstrated by genetic interactions with other autophagy genes (unc-51/ATG1, etc.) and the daf-2 insulin signaling pathway.
Reason: This is the core biological process for BEC-1. Strong genetic evidence from the foundational autophagy study in C. elegans.
Supporting Evidence:
PMID:12958363
bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension
GO:0008340 determination of adult lifespan
IGI
PMID:12958363
Autophagy genes are essential for dauer development and life... 		ACCEPT
Summary: bec-1 is required for lifespan extension in daf-2/insulin signaling mutants.
Reason: Foundational study demonstrating autophagy requirement for insulin signaling-mediated longevity.
Supporting Evidence:
PMID:12958363
bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension
GO:0040024 dauer larval development
IGI
PMID:12958363
Autophagy genes are essential for dauer development and life... 		ACCEPT
Summary: bec-1 is essential for normal dauer morphogenesis. RNAi knockdown causes abnormalities in constitutive dauer formation in daf-2 mutants.
Reason: Well-documented role of bec-1 in dauer development, which requires autophagy for proper morphogenesis and survival.
Supporting Evidence:
PMID:12958363
bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis

Core Functions

BEC-1 functions as a scaffold/adaptor within class III PI3K complexes, bridging the VPS-34 catalytic kinase with complex-specific subunits (EPG-8/ATG14 for autophagy, UVRAG for endocytosis) and regulatory proteins (SORF-1/2, CED-9).

Molecular Function:
protein-macromolecule adaptor activity

BEC-1 directly binds VPS-34, the class III PI3K catalytic subunit, enabling PtdIns3P production required for autophagy initiation and endosomal trafficking.

Molecular Function:
phosphatidylinositol 3-kinase binding

BEC-1 is essential for autophagosome nucleation as part of the PI3KC3-C1 complex, generating PtdIns3P at phagophore assembly sites.

Molecular Function:
protein-macromolecule adaptor activity
Directly Involved In:
autophagosome assembly
In Complex:
phosphatidylinositol 3-kinase complex, class III, type I

BEC-1 functions in endocytic trafficking through the PI3KC3-C2 complex, regulating endosome maturation and retrograde transport.

Molecular Function:
protein-macromolecule adaptor activity
Directly Involved In:
endocytosis
In Complex:
phosphatidylinositol 3-kinase complex, class III, type II

References

GO_REF:0000033
Annotation inferences using phylogenetic trees
  • IBA annotations based on PANTHER phylogenetic trees inferring function from characterized orthologs
GO_REF:0000043
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
GO_REF:0000044
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping
GO_REF:0000120
Combined Automated Annotation using Multiple IEA Methods
PMID:12958363
Autophagy genes are essential for dauer development and life-span extension in C. elegans.
  • BEC-1 is required for autophagy, dauer morphogenesis, and lifespan extension
    "bec-1, the C. elegans ortholog of the yeast and mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal dauer morphogenesis and life-span extension"
  • Foundational paper establishing autophagy requirement in C. elegans longevity
    "Dauer formation is associated with increased autophagy and also requires C. elegans orthologs of the yeast autophagy genes APG1, APG7, APG8, and AUT10"
PMID:16111945
Inactivation of the autophagy gene bec-1 triggers apoptotic cell death in C. elegans.
  • BEC-1 is essential for development and necessary for VPS-34/LET-512 function
    "BEC-1, the C. elegans ortholog of the yeast and mammalian autophagy proteins Atg6/Vps30 and Beclin 1, is essential for development"
  • BEC-1 forms a complex with CED-9/BCL-2 and regulates apoptosis
    "BEC-1 forms a complex with the antiapoptotic protein CED-9/Bcl-2, and its depletion triggers CED-3/Caspase-dependent PCD"
PMID:17172799
Autophagy genes protect against disease caused by polyglutamine expansion proteins in Caenorhabditis elegans.
  • Autophagy genes including bec-1 protect against polyQ toxicity
    "genetic inactivation of autophagy genes accelerates the accumulation of polyQ40 aggregates in C. elegans muscle cells"
PMID:17327275
Influence of autophagy genes on ion-channel-dependent neuronal degeneration in Caenorhabditis elegans.
  • bec-1 contributes to ion-channel-dependent neurotoxicity
    "Inactivation of unc-51, bec-1 and lgg-1, the worm counterparts of the yeast autophagy genes Atg1, Atg6 and Atg8 respectively, partially suppresses degeneration of neurons with toxic ion channel variants"
PMID:17785524
Dual roles of autophagy in the survival of Caenorhabditis elegans during starvation.
  • Physiological autophagy promotes starvation survival
    "we show that physiological levels of autophagy act to promote survival in Caenorhabditis elegans during starvation"
PMID:17890369
Autophagy genes unc-51 and bec-1 are required for normal cell size in Caenorhabditis elegans.
  • bec-1 mutants have small body size
    "mutational inactivation of two autophagy genes unc-51/atg1 and bec-1/atg6/beclin1 results in small body size without affecting cell number"
PMID:17912023
Autophagy is required for dietary restriction-mediated life span extension in C. elegans.
  • bec-1 is required for dietary restriction longevity in eat-2 mutants
    "two essential autophagy genes (bec-1 and Ce-atg7) are required for the longevity phenotype of the C. elegans dietary restriction mutant"
PMID:21116129
The coiled-coil domain protein EPG-8 plays an essential role in the autophagy pathway in C. elegans.
  • EPG-8 directly interacts with BEC-1
    "EPG-8 directly interacts with the C. elegans Beclin 1 homolog, BEC-1"
  • EPG-8 functions as C. elegans ATG14 homolog
    "Our study demonstrates that epg-8 may function as a highly divergent homolog of the yeast autophagy gene Atg14"
PMID:21183797
The Atg6/Vps30/Beclin 1 ortholog BEC-1 mediates endocytic retrograde transport in addition to autophagy in C. elegans.
  • BEC-1 functions in endosome-to-Golgi retrograde transport
    "we report that BEC-1, the C. elegans ortholog of Atg6/Vps30/Beclin1, a key regulator of the autophagic machinery, also contributes to endosome function"
  • BEC-1 is required for apoptotic corpse clearance
    "We further identify a requirement for BEC-1 in the clearance of apoptotic corpses in the hermaphrodite gonad, suggesting a role for BEC-1 in phagosome maturation"
PMID:21906946
Autophagy and lipid metabolism coordinately modulate life span in germline-less C. elegans.
  • Autophagy required for germline-less longevity
    "Germline removal extends life span in C. elegans via genes such as the lipase LIPL-4"
PMID:26783301
Negative regulation of phosphatidylinositol 3-phosphate levels in early-to-late endosome conversion.
  • BEC-1 is part of the PI3K complex that generates PtdIns3P
    "SORF-1 and SORF-2 act in a complex with BEC-1/Beclin1"
  • SORF-1 and SORF-2 interact with BEC-1 to regulate PI3K activity
    "Loss of sorf-1 or sorf-2 leads to greatly elevated endosomal PtdIns3P, which drives excessive fusion of early endosomes"
PMID:28285998
A Non-Cell-Autonomous Role of BEC-1/BECN1/Beclin1 in Coordinating Cell-Cycle Progression and Stem Cell Proliferation during Germline Development.
  • BEC-1 required for germline stem cell proliferation
    "We found that autophagy genes such as bec-1/BECN1/Beclin1, atg-16.2/ATG16L, atg-18/WIPI1/2, and atg-7/ATG7 are required for the late larval expansion of germline stem cell progenitors"
  • Acts non-cell-autonomously
    "we report that BEC-1/BECN1/Beclin1 functions non-cell-autonomously to facilitate cell-cycle progression and stem cell proliferation"
file:worm/bec-1/bec-1-deep-research-falcon.md
Deep research on bec-1 gene function
  • BEC-1 functions as scaffold/adaptor for PI3KC3 complexes
    "BEC-1 functions primarily as a scaffold/adaptor for class III PI3K complexes (VPS-34 with VPS-15)"

Suggested Questions for Experts

Q: Does BEC-1 have distinct pools for autophagy versus endocytosis functions?

Q: What regulates the balance between PI3KC3-C1 and PI3KC3-C2 complex formation?

Q: Is the nuclear localization of BEC-1 functionally significant?

Suggested Experiments

Experiment: Tissue-specific rescue experiments to determine which tissues require BEC-1 for different phenotypes

Experiment: Structure-function analysis to identify domains required for different protein interactions

Experiment: Live imaging of BEC-1 dynamics during autophagy induction versus endosome maturation

Tags

caeel-proteostasis caeel-mitophagy

📚 Additional Documentation

Deep Research Falcon

(bec-1-deep-research-falcon.md)

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gene_id: bec-1
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protein_description: 'RecName: Full=Beclin homolog {ECO:0000312|WormBase:T19E7.3a};'
gene_info: Name=bec-1 {ECO:0000312|WormBase:T19E7.3a}; Synonyms=atg-6 {ECO:0000312|WormBase:T19E7.3a};
ORFNames=T19E7.3 {ECO:0000312|WormBase:T19E7.3a};
organism_full: Caenorhabditis elegans.
protein_family: Belongs to the beclin family. .
protein_domains: Atg6/Beclin. (IPR007243); Atg6/Beclin_C_sf. (IPR038274); Atg6/beclin_CC.
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Question

Gene Research for Functional Annotation

⚠️ CRITICAL: Gene/Protein Identification Context

BEFORE YOU BEGIN RESEARCH: You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

Target Gene/Protein Identity (from UniProt):

  • UniProt Accession: Q22592
  • Protein Description: RecName: Full=Beclin homolog {ECO:0000312|WormBase:T19E7.3a};
  • Gene Information: Name=bec-1 {ECO:0000312|WormBase:T19E7.3a}; Synonyms=atg-6 {ECO:0000312|WormBase:T19E7.3a}; ORFNames=T19E7.3 {ECO:0000312|WormBase:T19E7.3a};
  • Organism (full): Caenorhabditis elegans.
  • Protein Family: Belongs to the beclin family. .
  • Key Domains: Atg6/Beclin. (IPR007243); Atg6/Beclin_C_sf. (IPR038274); Atg6/beclin_CC. (IPR041691); Atg6_BARA. (IPR040455); APG6 (PF04111)

MANDATORY VERIFICATION STEPS:

  1. Check if the gene symbol "bec-1" matches the protein description above
  2. Verify the organism is correct: Caenorhabditis elegans.
  3. Check if protein family/domains align with what you find in literature
  4. If you find literature for a DIFFERENT gene with the same or similar symbol, STOP

If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE. Instead:
- State clearly: "The gene symbol 'bec-1' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

Research Target:

Please provide a comprehensive research report on the gene bec-1 (gene ID: bec-1, UniProt: Q22592) in worm.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Output

Question: You are an expert researcher providing comprehensive, well-cited information.

Provide detailed information focusing on:
1. Key concepts and definitions with current understanding
2. Recent developments and latest research (prioritize 2023-2024 sources)
3. Current applications and real-world implementations
4. Expert opinions and analysis from authoritative sources
5. Relevant statistics and data from recent studies

Format as a comprehensive research report with proper citations. Include URLs and publication dates where available.
Always prioritize recent, authoritative sources and provide specific citations for all major claims.

Gene Research for Functional Annotation

⚠️ CRITICAL: Gene/Protein Identification Context

BEFORE YOU BEGIN RESEARCH: You MUST verify you are researching the CORRECT gene/protein. Gene symbols can be ambiguous, especially for less well-characterized genes from non-model organisms.

Target Gene/Protein Identity (from UniProt):

  • UniProt Accession: Q22592
  • Protein Description: RecName: Full=Beclin homolog {ECO:0000312|WormBase:T19E7.3a};
  • Gene Information: Name=bec-1 {ECO:0000312|WormBase:T19E7.3a}; Synonyms=atg-6 {ECO:0000312|WormBase:T19E7.3a}; ORFNames=T19E7.3 {ECO:0000312|WormBase:T19E7.3a};
  • Organism (full): Caenorhabditis elegans.
  • Protein Family: Belongs to the beclin family. .
  • Key Domains: Atg6/Beclin. (IPR007243); Atg6/Beclin_C_sf. (IPR038274); Atg6/beclin_CC. (IPR041691); Atg6_BARA. (IPR040455); APG6 (PF04111)

MANDATORY VERIFICATION STEPS:

  1. Check if the gene symbol "bec-1" matches the protein description above
  2. Verify the organism is correct: Caenorhabditis elegans.
  3. Check if protein family/domains align with what you find in literature
  4. If you find literature for a DIFFERENT gene with the same or similar symbol, STOP

If Gene Symbol is Ambiguous or You Cannot Find Relevant Literature:

DO NOT PROCEED WITH RESEARCH ON A DIFFERENT GENE. Instead:
- State clearly: "The gene symbol 'bec-1' is ambiguous or literature is limited for this specific protein"
- Explain what you found (e.g., "Found extensive literature on a different gene with the same symbol in a different organism")
- Describe the protein based ONLY on the UniProt information provided above
- Suggest that the protein function can be inferred from domain/family information

Research Target:

Please provide a comprehensive research report on the gene bec-1 (gene ID: bec-1, UniProt: Q22592) in worm.

The research report should be a detailed narrative explaining the function, biological processes, and localization of the gene product. Citations should be given for all claims.

You should prioritize authoritative reviews and primary scientific literature when conducting research. You can supplement
this with annotations you find in gene/protein databases, but these can be outdated or inaccurate.

We are specifically interested in the primary function of the gene - for enzymes, what reaction is catalyzed, and what is the substrate specificity? For transporters, what is the substrate? For structural proteins or adapters, what is the broader structural role? For signaling molecules, what is the role in the pathway.

We are interested in where in or outside the cell the gene product carries out its function.

We are also interested in the signaling or biochemical pathways in which the gene functions. We are less interested in broad pleiotropic effects, except where these elucidate the precise role.

Include evidence where possible. We are interested in both experimental evidence as well as inference from structure, evolution, or bioinformatic analysis. Precise studies should be prioritized over high-throughput, where available.

Plan
We verified the gene/protein identity and then synthesized recent, authoritative evidence on function, localization, pathway context, applications, and recent developments, prioritizing 2023–2024 literature in Caenorhabditis elegans.

Artifact summary
| Topic | Key points (1–2 sentences) | Source(s) [pqac IDs] | URL / Year |
|---|---|---:|---|
| Identity verification | bec-1 is the Caenorhabditis elegans ortholog of Atg6/Beclin (UniProt Q22592) and belongs to the Beclin/Atg6 protein family with conserved coiled-coil and BARA-like domains. | (konstantinidis2021molecularbasisof pages 7-8, maheshwari2025thebiologicalrole pages 3-5) | https://doi.org/10.3390/cells10030694 (2021); https://doi.org/10.20944/preprints202507.2396.v1 (2025) |
| Molecular function & complexes | BEC-1 functions primarily as a scaffold/adaptor for class III PI3K complexes (VPS-34 with VPS-15) that assemble with complex-specific partners (EPG-8/ATG-14 for autophagosome nucleation; VPS-38/UVRAG for endocytic maturation), enabling VPS-34 PI3P production rather than acting as the lipid kinase itself. | (maheshwari2025thebiologicalrole pages 3-5, swords2023aconservedrequirement pages 37-40, fazeli2016c.elegansmidbodies pages 20-22) | https://doi.org/10.20944/preprints202507.2396.v1 (2025); https://doi.org/10.1101/2023.02.27.530319 (2023); https://doi.org/10.1242/jcs.190223 (2016) |
| Cellular localization & dynamics | BEC-1 is recruited to ER/omegasome–phagophore sites, autophagosomes, phagosomes (LAP-associated) and autolysosomes; it localizes around internalized midbody/phagosomal membranes and is required for LGG-1/LGG-2 puncta formation and recruitment. | (fazeli2016c.elegansmidbodies pages 20-22, ploumi2023couplingofautophagy pages 6-7, konstantinidis2021molecularbasisof pages 7-8) | https://doi.org/10.1242/jcs.190223 (2016); https://doi.org/10.1038/s41419-023-05638-x (2023); https://doi.org/10.3390/cells10030694 (2021) |
| Pathway contexts | BEC-1 is essential for PI3KC3-dependent vesicle nucleation during canonical autophagy initiation, contributes to endocytic trafficking and LC3-associated phagocytosis (LAP), and participates in autolysosome reformation (ALR) required for maintaining lysosomal capacity. | (fazeli2016c.elegansmidbodies pages 20-22, ploumi2023couplingofautophagy pages 6-7, swords2023aconservedrequirement pages 37-40) | https://doi.org/10.1242/jcs.190223 (2016); https://doi.org/10.1038/s41419-023-05638-x (2023); https://doi.org/10.1101/2023.02.27.530319 (2023) |
| 2023–2024 C. elegans highlights | A 2023 study implicates bec-1 in neuronal autolysosome reformation and autolysosomal tubule regulation (ALR defects phenocopy bec-1 perturbation); 2023–2024 work links bec-1 loss/knockdown to altered lifespan and stress-resistance phenotypes in worm models. | (swords2023aconservedrequirement pages 37-40, ploumi2023couplingofautophagy pages 6-7, chung2024c.eleganshuntingtin pages 21-23) | https://doi.org/10.1101/2023.02.27.530319 (2023); https://doi.org/10.1038/s41419-023-05638-x (2023); https://doi.org/10.1101/2024.12.01.625591 (2024) |
| Experimental tools & reporters | Common approaches include RNAi and genetic alleles to knock down bec-1, GFP::BEC-1 and GFP::LGG-1 / plgg-1::GFP::LGG-1 reporters to monitor puncta and flux, and p62/SQST-1 cargo reporters or dFP-based flux assays to measure autophagic degradation. | (konstantinidis2021molecularbasisof pages 7-8, ploumi2023couplingofautophagy pages 6-7, chung2024c.eleganshuntingtin pages 21-23, fazeli2016c.elegansmidbodies pages 20-22) | https://doi.org/10.3390/cells10030694 (2021); https://doi.org/10.1038/s41419-023-05638-x (2023); https://doi.org/10.1101/2024.12.01.625591 (2024); https://doi.org/10.1242/jcs.190223 (2016) |

Table: Compact, evidence-backed summary of identity, function, localization, pathway roles, recent C. elegans findings (2023–2024), and common experimental tools for bec-1 (UniProt Q22592). Useful as a quick reference for experimental planning and literature review.

1) Key concepts and definitions (current understanding)
- Identity and family: bec-1 encodes the C. elegans ortholog of Beclin/Atg6 (yeast Vps30/Atg6), a core component of class III PI3K (PI3KC3/VPS-34) machinery. It belongs to the Beclin family and contains conserved coiled-coil and BARA-like domains that mediate complex assembly and membrane engagement; the worm identity and family membership match the UniProt specification (Organism: C. elegans). These features underpin a primary role as a scaffold/adaptor, not as the lipid kinase itself (VPS-34 is the enzyme) (konstantinidis2021molecularbasisof pages 7-8, maheshwari2025thebiologicalrole pages 3-5).
- PI3KC3 complexes: BEC-1 assembles with VPS-34 and VPS-15, plus complex-defining subunits to form PI3KC3-C1 (with ATG14/EPG-8) for autophagosome nucleation and PI3KC3-C2 (with UVRAG-like/VPS-38) for endocytic/endolysosomal maturation. In C. elegans, these assignments are supported by genetic and cell-biological studies linking BEC-1 to autophagy initiation and endocytic trafficking (swords2023aconservedrequirement pages 37-40, maheshwari2025thebiologicalrole pages 3-5, fazeli2016c.elegansmidbodies pages 20-22).
- Canonical vs noncanonical roles: Beyond canonical macroautophagy initiation, BEC-1 participates in LC3-associated phagocytosis (LAP) and phagosome maturation in vivo, reflecting noncanonical deployment of core autophagy proteins in single-membrane trafficking processes (fazeli2016c.elegansmidbodies pages 20-22).

2) Recent developments and latest research (emphasis 2023–2024)
- Neuronal autolysosome reformation (ALR): 2023 in vivo work shows that perturbing PI3KC3 components in C. elegans neurons (including bec-1/beclin and vps-15) causes accumulation of elongated autolysosomal tubules and reduced autophagic flux, implicating bec-1 in ALR and clathrin-dependent regulation of autolysosomal tubules (swords2023aconservedrequirement pages 37-40).
- Autophagy–apoptosis coupling in ageing: 2023 data link autophagy to longevity via mitochondrial apoptosis regulators; inhibition of autophagy by bec-1(RNAi) blunts lifespan extension phenotypes in genetic models, supporting a functional requirement for BEC-1-mediated autophagy in pro-longevity pathways (ploumi2023couplingofautophagy pages 6-7).
- Stress and infection responses: 2024 preprint evidence uses bec-1 RNAi as a core autophagy control in models of stress resistance and infection, reinforcing the standard role of bec-1 in autophagy induction during physiological challenge in worms (chung2024c.eleganshuntingtin pages 21-23).

3) Current applications and real-world implementations
- Genetic perturbation: bec-1(RNAi) and loss-of-function alleles are routine to inhibit autophagy in vivo for lifespan studies, neuronal trafficking, and stress-resistance assays; these manipulations predictably reduce autophagic flux and can negate longevity phenotypes contingent on autophagy (ploumi2023couplingofautophagy pages 6-7, konstantinidis2021molecularbasisof pages 7-8).
- Imaging reporters and flux assays: GFP::LGG-1 (LC3 family) reporters (plgg-1::GFP::LGG-1) monitor puncta and flux; BEC-1 localization and function are inferred from LGG-1/2 dynamics and from BEC-1::GFP enrichment at phagosomes. These tools are deployed in neuronal ALR studies and phagosome maturation/LAP analyses (swords2023aconservedrequirement pages 37-40, fazeli2016c.elegansmidbodies pages 20-22, ploumi2023couplingofautophagy pages 6-7).
- Physiological phenotyping: Autophagy-dependent phenotypes (e.g., lifespan modulation, proteostasis, infection survival, neuronal autolysosome dynamics) are interrogated with bec-1 perturbations to establish causal roles of autophagy in whole-animal physiology (ploumi2023couplingofautophagy pages 6-7, chung2024c.eleganshuntingtin pages 21-23).

4) Expert opinions and analysis (authoritative sources)
- Consensus view: Authoritative reviews and syntheses position BEC-1 as a central scaffold of PI3KC3 complexes controlling autophagosome nucleation and endolysosomal traffic; conserved domain architecture underlies its partnership with VPS-34/VPS-15 and complex-specific adaptors (maheshwari2025thebiologicalrole pages 3-5).
- Worm-specific context: Reviews focused on neuronal autophagy and ageing in C. elegans emphasize that bec-1 (with vps-34, vps-15, epg-8/ATG14) executes vesicle nucleation, and that autophagy genes including bec-1 are required for longevity in classic insulin/IGF-1 pathway mutants (konstantinidis2021molecularbasisof pages 7-8).
- Noncanonical autophagy: In vivo cell-biology evidence in C. elegans supports noncanonical roles (LAP) for BEC-1 and LGG-1/2 in the degradation of phagosomal cargo (midbodies), expanding the scope of Beclin-dependent membrane processing (fazeli2016c.elegansmidbodies pages 20-22).

5) Relevant statistics and data from recent studies
- Neuronal ALR phenotypes: Loss of bec-1/beclin in C. elegans neurons leads to accumulation of grossly elongated autolysosomal tubules and lowered autophagic flux; ALR defects are shared with other PI3KC3 regulators (e.g., vps-15), indicating a conserved requirement of BEC-1 for ALR (qualitative neuronal phenotypes reported with fluorescence markers) (swords2023aconservedrequirement pages 37-40).
- Lifespan dependence on BEC-1: In genetic combinations that extend lifespan via mitochondrial apoptosis pathway modulation, autophagy suppression by bec-1(RNAi) eliminates the lifespan extension, indicating quantitative lifespan outcomes depend on intact BEC-1-mediated autophagy (qualitative conclusion; exact lifespans reported in the study’s figures) (ploumi2023couplingofautophagy pages 6-7).
- LAP/phagosome maturation: BEC-1::GFP is enriched around internalized midbody phagosomes; BEC-1 and LGG-1/LGG-2 are required for timely midbody degradation, consistent with a requirement for PI3KC3 activity in single-membrane phagosome processing (qualitative imaging and dependency data) (fazeli2016c.elegansmidbodies pages 20-22).

Functional annotation of bec-1 (Q22592)
- Primary molecular role: BEC-1 is a scaffold/adaptor within class III PI3K complexes. In PI3KC3-C1 (VPS-34–VPS-15–EPG-8/ATG14–BEC-1), it promotes autophagosome nucleation by positioning VPS-34 to generate PI3P at ER-derived omegasomes and nascent phagophores. In PI3KC3-C2 (VPS-34–VPS-15–VPS-38/UVRAG–BEC-1), it supports endocytic/phagosomal maturation and endolysosomal trafficking, including LAP and ALR (maheshwari2025thebiologicalrole pages 3-5, fazeli2016c.elegansmidbodies pages 20-22, swords2023aconservedrequirement pages 37-40).
- Not an enzyme: BEC-1 does not catalyze lipid phosphorylation; VPS-34 is the PI3P-generating kinase. BEC-1’s domains mediate partner selection and membrane targeting, regulating VPS-34 activity and pathway specificity (maheshwari2025thebiologicalrole pages 3-5).
- Subcellular localization: BEC-1 localizes to ER-associated omegasomes/phagophores during autophagy initiation, to autophagosomes, and to single-membrane phagosomes during LAP; it is also implicated at autolysosomes during ALR in neurons (fazeli2016c.elegansmidbodies pages 20-22, ploumi2023couplingofautophagy pages 6-7, swords2023aconservedrequirement pages 37-40).
- Pathways: BEC-1 acts at the vesicle nucleation stage of macroautophagy, contributes to endocytic trafficking and phagosome maturation (LAP), and is required for autolysosome reformation to sustain lysosomal capacity, particularly in neurons (fazeli2016c.elegansmidbodies pages 20-22, swords2023aconservedrequirement pages 37-40).

Experimental evidence and tools
- Genetic models: bec-1 loss-of-function or RNAi is used to inhibit autophagy; genetic epistasis demonstrates that longevity phenotypes and stress-resistance gains often require bec-1 (ploumi2023couplingofautophagy pages 6-7, chung2024c.eleganshuntingtin pages 21-23).
- Imaging reporters: plgg-1::GFP::LGG-1 reporters quantify autophagic puncta/flux; BEC-1::GFP enriches at phagosome rims (midbodies) and autophagy-associated membranes; neuronal ALR studies use autolysosomal tubule reporters to diagnose ALR defects upon bec-1 perturbation (fazeli2016c.elegansmidbodies pages 20-22, swords2023aconservedrequirement pages 37-40, ploumi2023couplingofautophagy pages 6-7).

Notes on verification and ambiguity
- Symbol and organism verification: The gene symbol bec-1 in Caenorhabditis elegans corresponds to UniProt Q22592 (Beclin homolog). Literature cited above consistently uses bec-1 as the C. elegans Beclin/ATG6 ortholog; no conflicting usage was identified during this review (konstantinidis2021molecularbasisof pages 7-8).

Conclusion
C. elegans bec-1 (Q22592) encodes the conserved Beclin/ATG6 scaffold that directs VPS-34 lipid kinase activity within PI3KC3 complexes to regulate autophagosome nucleation, noncanonical phagosome maturation (LAP), and neuronal autolysosome reformation. Recent 2023 in vivo studies highlight bec-1’s specific requirement for ALR and show that genetic longevity/stress phenotypes are bec-1-dependent, reaffirming its central, adaptor-mediated role across canonical and noncanonical membrane remodeling pathways in vivo (swords2023aconservedrequirement pages 37-40, fazeli2016c.elegansmidbodies pages 20-22, ploumi2023couplingofautophagy pages 6-7).

References

  1. (konstantinidis2021molecularbasisof pages 7-8): Georgios Konstantinidis and Nektarios Tavernarakis. Molecular basis of neuronal autophagy in ageing: insights from caenorhabditis elegans. Cells, 10:694, Mar 2021. URL: https://doi.org/10.3390/cells10030694, doi:10.3390/cells10030694. This article has 19 citations and is from a poor quality or predatory journal.

  2. (maheshwari2025thebiologicalrole pages 3-5): Chinmay Maheshwari, Andrea Castiglioni, Uthman Walusimbi, Chiara Vidoni, Alessandra Ferraresi, Danny N. Dhanasekaran, and Ciro Isidoro. The biological role and clinical significance of beclin-1 in cancer. Jul 2025. URL: https://doi.org/10.20944/preprints202507.2396.v1, doi:10.20944/preprints202507.2396.v1.

  3. (swords2023aconservedrequirement pages 37-40): Sierra Swords, Nuo Jia, Anne Norris, Jil Modi, Qian Cai, and Barth D. Grant. A conserved requirement for rme-8/dnajc13 in neuronal autolysosome reformation. bioRxiv, Feb 2023. URL: https://doi.org/10.1101/2023.02.27.530319, doi:10.1101/2023.02.27.530319. This article has 4 citations and is from a poor quality or predatory journal.

  4. (fazeli2016c.elegansmidbodies pages 20-22): Gholamreza Fazeli, Michaela Trinkwalder, Linda Irmisch, and Ann Marie Wehman. C. elegans midbodies are released, phagocytosed and undergo lc3-dependent degradation independent of macroautophagy. Journal of Cell Science, 129:3721-3731, Oct 2016. URL: https://doi.org/10.1242/jcs.190223, doi:10.1242/jcs.190223. This article has 63 citations and is from a domain leading peer-reviewed journal.

  5. (ploumi2023couplingofautophagy pages 6-7): Christina Ploumi, Emmanouil Kyriakakis, and Nektarios Tavernarakis. Coupling of autophagy and the mitochondrial intrinsic apoptosis pathway modulates proteostasis and ageing in caenorhabditis elegans. Cell Death & Disease, Feb 2023. URL: https://doi.org/10.1038/s41419-023-05638-x, doi:10.1038/s41419-023-05638-x. This article has 32 citations and is from a peer-reviewed journal.

  6. (chung2024c.eleganshuntingtin pages 21-23): Christine Hyein Chung, Hanee Lee, Kyumin Park, Young Seo Park, Roy Jung, Ihnsik Seong, and Junho Lee. C. elegans huntingtin, htt-1, promotes robust autophagy induction and survival under stress conditions. bioRxiv, Dec 2024. URL: https://doi.org/10.1101/2024.12.01.625591, doi:10.1101/2024.12.01.625591. This article has 0 citations and is from a poor quality or predatory journal.

Citations

  1. swords2023aconservedrequirement pages 37-40
  2. ploumi2023couplingofautophagy pages 6-7
  3. maheshwari2025thebiologicalrole pages 3-5
  4. konstantinidis2021molecularbasisof pages 7-8
  5. pqac IDs
  6. https://doi.org/10.3390/cells10030694
  7. https://doi.org/10.20944/preprints202507.2396.v1
  8. https://doi.org/10.1101/2023.02.27.530319
  9. https://doi.org/10.1242/jcs.190223
  10. https://doi.org/10.1038/s41419-023-05638-x
  11. https://doi.org/10.1101/2024.12.01.625591
  12. https://doi.org/10.3390/cells10030694,
  13. https://doi.org/10.20944/preprints202507.2396.v1,
  14. https://doi.org/10.1101/2023.02.27.530319,
  15. https://doi.org/10.1242/jcs.190223,
  16. https://doi.org/10.1038/s41419-023-05638-x,
  17. https://doi.org/10.1101/2024.12.01.625591,

📄 View Raw YAML

 
id: Q22592
gene_symbol: bec-1
product_type: PROTEIN
status: COMPLETE
taxon:
  id: NCBITaxon:6239
  label: Caenorhabditis elegans
description: BEC-1 is the C. elegans ortholog of yeast Atg6/Vps30 and mammalian 
  Beclin-1, functioning as an essential scaffold/adaptor subunit of the class 
  III phosphatidylinositol 3-kinase (PI3K) complex. BEC-1 assembles with VPS-34 
  (the catalytic PI3K subunit) and VPS-15 to form complexes that generate 
  phosphatidylinositol 3-phosphate (PtdIns3P) on membranes. In the PI3KC3-C1 
  complex (with EPG-8/ATG14), BEC-1 promotes autophagosome nucleation at 
  ER-derived omegasomes. In the PI3KC3-C2 complex (with UVRAG/VPS-38), BEC-1 
  supports endocytic trafficking, endosome-to-Golgi retrograde transport, and 
  phagosome maturation. BEC-1 also interacts with CED-9 (BCL-2 family) to 
  negatively regulate apoptosis. The protein is essential for dauer 
  morphogenesis, lifespan extension in insulin signaling mutants, survival 
  during starvation, clearance of apoptotic corpses, germline stem cell 
  proliferation, and protection against protein aggregation toxicity.
existing_annotations:
  - term:
      id: GO:0000045
      label: autophagosome assembly
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: BEC-1 is a core component of the PI3KC3-C1 complex that initiates
        autophagosome formation. Evidence from PMID:12958363 demonstrates that 
        bec-1 is essential for autophagosome formation in seam cells during 
        dauer development. BEC-1 functions with VPS-34 to generate PtdIns3P at 
        phagophore assembly sites, which is required for recruitment of 
        downstream autophagy machinery including LGG-1/LC3.
      action: ACCEPT
      reason: This is a core molecular function of BEC-1 as the Beclin ortholog.
        Multiple studies confirm BEC-1's essential role in autophagosome 
        assembly as part of the PI3KC3 complex.
      supported_by:
        - reference_id: PMID:12958363
          supporting_text: bec-1, the C. elegans ortholog of the yeast and 
            mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal
            dauer morphogenesis and life-span extension
        - reference_id: PMID:16111945
          supporting_text: We demonstrate that BEC-1 is necessary for the 
            function of the class III PI3 kinase LET-512/Vps34, an essential 
            protein required for autophagy
  - term:
      id: GO:0000423
      label: mitophagy
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: Mitophagy is a selective form of autophagy that degrades 
        mitochondria. While BEC-1 is essential for general autophagy, there is 
        limited direct experimental evidence specifically demonstrating BEC-1's 
        role in mitophagy in C. elegans. The IBA annotation is based on 
        phylogenetic inference from mammalian Beclin-1.
      action: ACCEPT
      reason: As a core component of the autophagy initiation complex, BEC-1 
        would be required for mitophagy, which is a selective form of 
        macroautophagy. The phylogenetic inference is sound given the conserved 
        role of Beclin/Atg6 proteins in all forms of autophagy.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-deep-research-falcon.md
          supporting_text: BEC-1 functions primarily as a scaffold/adaptor for 
            class III PI3K complexes (VPS-34 with VPS-15) that assemble with 
            complex-specific partners
  - term:
      id: GO:0030674
      label: protein-macromolecule adaptor activity
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: BEC-1 functions as a scaffold/adaptor within the PI3KC3 complex, 
        bridging VPS-34 (the catalytic kinase) with other complex components 
        (EPG-8/ATG14, UVRAG) and regulatory proteins (CED-9, SORF-1, SORF-2). 
        BEC-1 does not have enzymatic activity itself but positions VPS-34 to 
        generate PtdIns3P at appropriate membrane sites.
      action: ACCEPT
      reason: This accurately describes BEC-1's primary molecular function. 
        BEC-1 serves as an adaptor between the VPS-34 kinase and other complex 
        components, consistent with the Beclin family's role across eukaryotes.
      supported_by:
        - reference_id: PMID:16111945
          supporting_text: Furthermore, BEC-1 forms a complex with the 
            antiapoptotic protein CED-9/Bcl-2
        - reference_id: PMID:21116129
          supporting_text: EPG-8 directly interacts with the C. elegans Beclin 1
            homolog, BEC-1
  - term:
      id: GO:0043548
      label: phosphatidylinositol 3-kinase binding
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: BEC-1 directly binds VPS-34, the class III PI3K catalytic 
        subunit, forming the core of the PI3KC3 complex. This interaction is 
        essential for VPS-34 function in both autophagy and endocytic 
        trafficking.
      action: ACCEPT
      reason: Direct experimental evidence from C. elegans confirms BEC-1 binds 
        VPS-34. This is a fundamental aspect of BEC-1 molecular function.
      supported_by:
        - reference_id: PMID:16111945
          supporting_text: We demonstrate that BEC-1 is necessary for the 
            function of the class III PI3 kinase LET-512/Vps34
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Interacts with vps-34 (PubMed:16111945, 
            PubMed:26783301)
  - term:
      id: GO:0034271
      label: phosphatidylinositol 3-kinase complex, class III, type I
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: The class III PI3K complex type I (PI3KC3-C1) contains VPS-34, 
        VPS-15, Beclin, and ATG14 and functions specifically in autophagy 
        initiation. In C. elegans, BEC-1 interacts with EPG-8 (the ATG14 
        homolog) for autophagy-specific functions.
      action: ACCEPT
      reason: BEC-1 is confirmed to be part of the autophagy-specific PI3KC3 
        complex containing EPG-8/ATG14. The interaction between BEC-1 and EPG-8 
        has been experimentally demonstrated.
      supported_by:
        - reference_id: PMID:21116129
          supporting_text: EPG-8 directly interacts with the C. elegans Beclin 1
            homolog, BEC-1. Our study demonstrates that epg-8 may function as a 
            highly divergent homolog of the yeast autophagy gene Atg14
  - term:
      id: GO:0034272
      label: phosphatidylinositol 3-kinase complex, class III, type II
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: The class III PI3K complex type II (PI3KC3-C2) contains VPS-34, 
        VPS-15, Beclin, and UVRAG and functions in endocytic trafficking. BEC-1 
        has documented roles in endocytic retrograde transport and endosome 
        maturation consistent with PI3KC3-C2 function.
      action: ACCEPT
      reason: BEC-1's role in endocytic trafficking is well documented. Evidence
        shows BEC-1 functions in the endosome-specific PI3KC3-C2 complex.
      supported_by:
        - reference_id: PMID:21183797
          supporting_text: BEC-1, the C. elegans ortholog of Atg6/Vps30/Beclin1,
            a key regulator of the autophagic machinery, also contributes to 
            endosome function
        - reference_id: file:worm/bec-1/bec-1-deep-research-falcon.md
          supporting_text: In PI3KC3-C2 (VPS-34-VPS-15-VPS-38/UVRAG-BEC-1), it 
            supports endocytic/phagosomal maturation and endolysosomal 
            trafficking
  - term:
      id: GO:0000407
      label: phagophore assembly site
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: BEC-1 localizes to sites of autophagosome initiation (phagophore 
        assembly sites/PAS) where it functions with VPS-34 to generate PtdIns3P 
        required for autophagy initiation. The deep research indicates BEC-1 is 
        recruited to ER/omegasome-phagophore sites.
      action: ACCEPT
      reason: As an essential component of the autophagy initiation PI3KC3-C1 
        complex, BEC-1 must localize to phagophore assembly sites. This is 
        consistent with its role in autophagosome nucleation.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-deep-research-falcon.md
          supporting_text: BEC-1 localizes to ER-associated 
            omegasomes/phagophores during autophagy initiation, to 
            autophagosomes, and to single-membrane phagosomes during LAP
  - term:
      id: GO:0006995
      label: cellular response to nitrogen starvation
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: Autophagy is induced under nitrogen starvation conditions. While 
        general starvation response has been documented for bec-1, specific 
        nitrogen starvation response in C. elegans has not been directly 
        demonstrated. The annotation is based on phylogenetic inference.
      action: KEEP_AS_NON_CORE
      reason: While BEC-1 is clearly required for starvation survival 
        (PMID:17785524), the specific nitrogen starvation response is inferred 
        rather than directly demonstrated in C. elegans. Keep as non-core since 
        the broader starvation response annotation is more directly supported.
      supported_by:
        - reference_id: PMID:17785524
          supporting_text: Here we show that physiological levels of autophagy 
            act to promote survival in Caenorhabditis elegans during starvation
  - term:
      id: GO:0045324
      label: late endosome to vacuole transport
    evidence_type: IBA
    original_reference_id: GO_REF:0000033
    review:
      summary: BEC-1 functions in endosomal trafficking including the conversion
        of early to late endosomes and subsequent transport. The PI3KC3 complex 
        generates PtdIns3P required for endosome maturation and transport.
      action: ACCEPT
      reason: BEC-1's role in endosomal transport is well documented. Evidence 
        from PMID:26783301 shows BEC-1 is required for proper early-to-late 
        endosome conversion and transport.
      supported_by:
        - reference_id: PMID:21183797
          supporting_text: we report that BEC-1, the C. elegans ortholog of 
            Atg6/Vps30/Beclin1, a key regulator of the autophagic machinery, 
            also contributes to endosome function
  - term:
      id: GO:0005737
      label: cytoplasm
    evidence_type: IEA
    original_reference_id: GO_REF:0000044
    review:
      summary: BEC-1 is localized to the cytoplasm. This is consistent with 
        direct experimental evidence from PMID:16111945.
      action: ACCEPT
      reason: IDA evidence from PMID:16111945 confirms cytoplasmic localization.
        The IEA annotation is redundant but correct.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: 'SUBCELLULAR LOCATION: Cytoplasm {ECO:0000269|PubMed:16111945}'
  - term:
      id: GO:0005768
      label: endosome
    evidence_type: IEA
    original_reference_id: GO_REF:0000044
    review:
      summary: BEC-1 localizes to endosomes where it functions as part of the 
        PI3KC3-C2 complex in endocytic trafficking. Evidence from PMID:21183797 
        shows endosomal localization.
      action: ACCEPT
      reason: UniProt annotation based on experimental evidence from 
        PMID:21183797 confirms endosomal localization.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Endosome {ECO:0000269|PubMed:21183797}. 
            Note=Co-localizes with rme-8, a component of the retromer complex, 
            on endosomes
  - term:
      id: GO:0006897
      label: endocytosis
    evidence_type: IEA
    original_reference_id: GO_REF:0000043
    review:
      summary: BEC-1 is required for proper endocytosis and endosome function. 
        Loss of bec-1 impairs fluid phase endocytosis and endosome-to-Golgi 
        retrograde transport.
      action: ACCEPT
      reason: Multiple studies confirm BEC-1's role in endocytosis. This is a 
        well-established function of Beclin/Atg6 proteins.
      supported_by:
        - reference_id: PMID:16111945
          supporting_text: We demonstrate that BEC-1 is necessary for the 
            function of the class III PI3 kinase LET-512/Vps34, an essential 
            protein required for autophagy, membrane trafficking, and 
            endocytosis
  - term:
      id: GO:0006914
      label: autophagy
    evidence_type: IEA
    original_reference_id: GO_REF:0000120
    review:
      summary: BEC-1 is essential for autophagy. This is the core function of 
        Beclin/Atg6 family proteins across eukaryotes.
      action: ACCEPT
      reason: Autophagy is the primary biological process for which BEC-1 is 
        required. This is supported by extensive experimental evidence.
      supported_by:
        - reference_id: PMID:12958363
          supporting_text: bec-1, the C. elegans ortholog of the yeast and 
            mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal
            dauer morphogenesis and life-span extension
  - term:
      id: GO:0030424
      label: axon
    evidence_type: IEA
    original_reference_id: GO_REF:0000044
    review:
      summary: BEC-1 is expressed in neurons including axonal regions. 
        Expression in ventral nerve cord and nerve ring has been documented.
      action: ACCEPT
      reason: UniProt subcellular location annotation based on experimental 
        evidence showing BEC-1 expression in neurons.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Cell projection, axon {ECO:0000269|PubMed:17327275}
  - term:
      id: GO:0030425
      label: dendrite
    evidence_type: IEA
    original_reference_id: GO_REF:0000044
    review:
      summary: BEC-1 is expressed in neuronal cells including dendrites based on
        UniProt subcellular location annotation.
      action: ACCEPT
      reason: UniProt annotation based on experimental evidence of neuronal 
        expression.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Cell projection, dendrite 
            {ECO:0000269|PubMed:17327275}
  - term:
      id: GO:0043204
      label: perikaryon
    evidence_type: IEA
    original_reference_id: GO_REF:0000044
    review:
      summary: BEC-1 is localized to neuronal cell bodies (perikarya) based on 
        expression in neurons.
      action: ACCEPT
      reason: UniProt annotation supported by evidence of neuronal expression.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Perikaryon {ECO:0000269|PubMed:17327275}
  - term:
      id: GO:0005515
      label: protein binding
    evidence_type: IPI
    original_reference_id: PMID:26783301
    review:
      summary: BEC-1 binds to SORF-1 and SORF-2, which regulate PI3KC3 complex 
        activity. The interaction was demonstrated by co-immunoprecipitation and
        pull-down assays.
      action: MODIFY
      reason: The term 'protein binding' is too vague. BEC-1 specifically 
        functions as an adaptor within the PI3KC3 complex. The interaction with 
        SORF-1/2 is regulatory and should be captured by the adaptor activity 
        annotation.
      proposed_replacement_terms:
        - id: GO:0030674
          label: protein-macromolecule adaptor activity
      supported_by:
        - reference_id: PMID:26783301
          supporting_text: SORF-1 and SORF-2 act in a complex with BEC-1/Beclin1
  - term:
      id: GO:0036093
      label: germ cell proliferation
    evidence_type: IMP
    original_reference_id: PMID:28285998
    review:
      summary: BEC-1 is required for germline stem cell proliferation during 
        late larval and adult stages. RNAi knockdown of bec-1 reduces stem cell 
        proliferation in the germline.
      action: KEEP_AS_NON_CORE
      reason: This is a documented phenotype of bec-1 loss but represents a 
        pleiotropic developmental role rather than the core molecular function. 
        The study shows this is non-cell-autonomous.
      supported_by:
        - reference_id: PMID:28285998
          supporting_text: We found that autophagy genes such as 
            bec-1/BECN1/Beclin1, atg-16.2/ATG16L, atg-18/WIPI1/2, and atg-7/ATG7
            are required for the late larval expansion of germline stem cell 
            progenitors
  - term:
      id: GO:0042078
      label: germ-line stem cell division
    evidence_type: IMP
    original_reference_id: PMID:28285998
    review:
      summary: BEC-1 promotes cell-cycle progression and stem cell division in 
        the germline during development.
      action: KEEP_AS_NON_CORE
      reason: This is a developmental phenotype reflecting BEC-1's role in 
        cellular homeostasis rather than its core molecular function.
      supported_by:
        - reference_id: PMID:28285998
          supporting_text: we report that BEC-1/BECN1/Beclin1 functions 
            non-cell-autonomously to facilitate cell-cycle progression and stem 
            cell proliferation
  - term:
      id: GO:0048284
      label: organelle fusion
    evidence_type: IMP
    original_reference_id: PMID:26783301
    review:
      summary: BEC-1 is required for endosome fusion. Loss of bec-1 in 
        combination with SORF genes affects early endosome fusion events.
      action: MODIFY
      reason: The term is too general. The evidence specifically supports a role
        in endosome fusion/maturation, not organelle fusion broadly.
      proposed_replacement_terms:
        - id: GO:0015075
          label: early endosome to late endosome transport
      additional_reference_ids:
        - PMID:21183797
      supported_by:
        - reference_id: PMID:26783301
          supporting_text: Loss of sorf-1 or sorf-2 leads to greatly elevated 
            endosomal PtdIns3P, which drives excessive fusion of early endosomes
        - reference_id: PMID:21183797
          supporting_text: The Atg6/Vps30/Beclin 1 ortholog BEC-1 mediates 
            endocytic retrograde transport in addition to autophagy in C.
  - term:
      id: GO:0048284
      label: organelle fusion
    evidence_type: IGI
    original_reference_id: PMID:26783301
    review:
      summary: IGI evidence for organelle fusion based on genetic interactions 
        with SORF-1, SORF-2, and VPS-34.
      action: MODIFY
      reason: Same as above - term is too general for the specific endosomal 
        fusion role supported by the evidence.
      proposed_replacement_terms:
        - id: GO:0015075
          label: early endosome to late endosome transport
      supported_by:
        - reference_id: PMID:26783301
          supporting_text: sorf-1 and sorf-2 function coordinately with Rab 
            switching genes to inhibit synthesis of PtdIns3P, allowing its 
            turnover for endosome conversion
  - term:
      id: GO:0051036
      label: regulation of endosome size
    evidence_type: IGI
    original_reference_id: PMID:26783301
    review:
      summary: BEC-1 affects endosome size through its role in generating 
        PtdIns3P via the PI3KC3 complex. Genetic interactions with SORF-1/2 
        modulate endosome size.
      action: ACCEPT
      reason: This is well supported by evidence from PMID:26783301 showing that
        BEC-1 and SORF proteins regulate PtdIns3P levels which controls endosome
        size and fusion.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: Double knockout with either sorf-1 or sorf-2 results 
            in smaller endosomes and an irregular distribution pattern of 
            PtdIns3P in the cytoplasm (PubMed:26783301)
        - reference_id: PMID:26783301
          supporting_text: Negative regulation of phosphatidylinositol 
            3-phosphate levels in early-to-late endosome conversion.
  - term:
      id: GO:2000643
      label: positive regulation of early endosome to late endosome transport
    evidence_type: IGI
    original_reference_id: PMID:26783301
    review:
      summary: BEC-1 positively regulates early-to-late endosome conversion 
        through generating PtdIns3P required for endosome maturation.
      action: ACCEPT
      reason: Evidence clearly supports BEC-1's role in early-to-late endosome 
        conversion through PtdIns3P generation.
      supported_by:
        - reference_id: PMID:26783301
          supporting_text: These findings reveal a conserved mechanism that 
            controls appropriate PtdIns3P levels in early-to-late endosome 
            conversion
  - term:
      id: GO:0045138
      label: nematode male tail tip morphogenesis
    evidence_type: IMP
    original_reference_id: PMID:17890369
    review:
      summary: bec-1 mutants show defects in male tail ray pattern formation, 
        indicating a role in developmental morphogenesis.
      action: KEEP_AS_NON_CORE
      reason: This is a developmental phenotype that likely reflects BEC-1's 
        general role in autophagy/cellular homeostasis rather than a specific 
        function in male tail morphogenesis.
      supported_by:
        - reference_id: PMID:17890369
          supporting_text: mutational inactivation of two autophagy genes 
            unc-51/atg1 and bec-1/atg6/beclin1 results in small body size 
            without affecting cell number
  - term:
      id: GO:0008340
      label: determination of adult lifespan
    evidence_type: IGI
    original_reference_id: PMID:21906946
    review:
      summary: bec-1 is required for lifespan extension in germline-less 
        animals. Autophagy and lipid metabolism coordinately modulate lifespan 
        and both require bec-1.
      action: ACCEPT
      reason: BEC-1-dependent autophagy is required for multiple longevity 
        pathways including insulin signaling mutants, dietary restriction, and 
        germline-less animals. This is a well-documented phenotype.
      supported_by:
        - reference_id: PMID:21906946
          supporting_text: Germline removal extends life span in C. elegans via 
            genes such as the lipase LIPL-4; however, less is known of the 
            cellular basis for this life-span extension
  - term:
      id: GO:0043277
      label: apoptotic cell clearance
    evidence_type: IMP
    original_reference_id: PMID:21183797
    review:
      summary: BEC-1 is required for clearance of apoptotic cell corpses in the 
        gonad, likely through its role in phagosome maturation.
      action: ACCEPT
      reason: The evidence directly supports BEC-1's role in apoptotic cell 
        clearance through phagosome maturation. This represents a non-canonical 
        function of BEC-1 in single-membrane processing.
      supported_by:
        - reference_id: PMID:21183797
          supporting_text: We further identify a requirement for BEC-1 in the 
            clearance of apoptotic corpses in the hermaphrodite gonad, 
            suggesting a role for BEC-1 in phagosome maturation
  - term:
      id: GO:0005515
      label: protein binding
    evidence_type: IPI
    original_reference_id: PMID:21116129
    review:
      summary: BEC-1 directly interacts with EPG-8 (ATG14 homolog), which is 
        required for autophagy function.
      action: MODIFY
      reason: Protein binding is too vague. This interaction is part of BEC-1's 
        adaptor function within the PI3KC3-C1 complex.
      proposed_replacement_terms:
        - id: GO:0030674
          label: protein-macromolecule adaptor activity
      supported_by:
        - reference_id: PMID:21116129
          supporting_text: EPG-8 directly interacts with the C. elegans Beclin 1
            homolog, BEC-1
  - term:
      id: GO:0008340
      label: determination of adult lifespan
    evidence_type: IGI
    original_reference_id: PMID:17912023
    review:
      summary: bec-1 is required for dietary restriction-mediated lifespan 
        extension in eat-2 mutants.
      action: ACCEPT
      reason: Well-documented role of bec-1 in autophagy-dependent lifespan 
        extension.
      supported_by:
        - reference_id: PMID:17912023
          supporting_text: two essential autophagy genes (bec-1 and Ce-atg7) are
            required for the longevity phenotype of the C. elegans dietary 
            restriction mutant
  - term:
      id: GO:0009267
      label: cellular response to starvation
    evidence_type: IMP
    original_reference_id: PMID:17785524
    review:
      summary: BEC-1-dependent autophagy is induced during starvation and 
        promotes survival. Physiological levels of autophagy are required for 
        starvation survival.
      action: ACCEPT
      reason: Clear experimental evidence that bec-1-dependent autophagy is 
        required for starvation survival in C. elegans.
      supported_by:
        - reference_id: PMID:17785524
          supporting_text: we show that physiological levels of autophagy act to
            promote survival in Caenorhabditis elegans during starvation
  - term:
      id: GO:0040014
      label: regulation of multicellular organism growth
    evidence_type: IGI
    original_reference_id: PMID:17890369
    review:
      summary: bec-1 mutants affect body size. Loss-of-function mutations in 
        unc-51 and bec-1 suppress the giant phenotype of insulin/IGF-1 and 
        TGF-beta signaling mutants.
      action: KEEP_AS_NON_CORE
      reason: This reflects BEC-1's role in cellular homeostasis affecting 
        organism growth, rather than a direct regulatory function.
      supported_by:
        - reference_id: PMID:17890369
          supporting_text: mutational inactivation of two autophagy genes 
            unc-51/atg1 and bec-1/atg6/beclin1 results in small body size 
            without affecting cell number
  - term:
      id: GO:0030163
      label: protein catabolic process
    evidence_type: IMP
    original_reference_id: PMID:17172799
    review:
      summary: BEC-1-dependent autophagy promotes clearance of polyglutamine 
        protein aggregates. Inactivation of autophagy genes accelerates 
        accumulation of polyQ aggregates.
      action: ACCEPT
      reason: Autophagy-dependent protein degradation is a core function of 
        BEC-1. Clear evidence for role in polyQ aggregate clearance.
      supported_by:
        - reference_id: PMID:17172799
          supporting_text: genetic inactivation of autophagy genes accelerates 
            the accumulation of polyQ40 aggregates in C. elegans muscle cells
  - term:
      id: GO:0012501
      label: programmed cell death
    evidence_type: IGI
    original_reference_id: PMID:17327275
    review:
      summary: bec-1 modulates necrotic cell death in neurons with hyperactive 
        ion channels. Inactivation of bec-1 partially suppresses degeneration of
        neurons with toxic ion channel variants.
      action: ACCEPT
      reason: Evidence shows bec-1 contributes to necrotic cell death in 
        specific contexts. Also, BEC-1 interacts with CED-9 to regulate 
        apoptosis.
      supported_by:
        - reference_id: PMID:17327275
          supporting_text: Inactivation of unc-51, bec-1 and lgg-1, the worm 
            counterparts of the yeast autophagy genes Atg1, Atg6 and Atg8 
            respectively, partially suppresses degeneration of neurons with 
            toxic ion channel variants
        - reference_id: PMID:16111945
          supporting_text: BEC-1 forms a complex with the antiapoptotic protein 
            CED-9/Bcl-2, and its depletion triggers CED-3/Caspase-dependent PCD
  - term:
      id: GO:0005634
      label: nucleus
    evidence_type: IDA
    original_reference_id: PMID:16111945
    review:
      summary: BEC-1 was detected in the nucleus by direct experimental 
        observation. This may represent a regulatory or signaling role.
      action: ACCEPT
      reason: Direct experimental evidence (IDA) from PMID:16111945.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: IDA:WormBase. Cytoplasm. Nucleus. Cytoplasmic vesicle
        - reference_id: PMID:16111945
          supporting_text: Inactivation of the autophagy gene bec-1 triggers 
            apoptotic cell death in C.
  - term:
      id: GO:0005737
      label: cytoplasm
    evidence_type: IDA
    original_reference_id: PMID:16111945
    review:
      summary: BEC-1 is localized to the cytoplasm where it functions in 
        autophagy and endosomal trafficking.
      action: ACCEPT
      reason: Direct experimental evidence (IDA) from PMID:16111945.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: 'SUBCELLULAR LOCATION: Cytoplasm {ECO:0000269|PubMed:16111945}'
        - reference_id: PMID:16111945
          supporting_text: Inactivation of the autophagy gene bec-1 triggers 
            apoptotic cell death in C.
  - term:
      id: GO:0031410
      label: cytoplasmic vesicle
    evidence_type: IDA
    original_reference_id: PMID:16111945
    review:
      summary: BEC-1 localizes to cytoplasmic vesicles including autophagosomes 
        and endosomes.
      action: ACCEPT
      reason: Direct experimental evidence (IDA) consistent with BEC-1's 
        function at autophagosomal and endosomal membranes.
      supported_by:
        - reference_id: file:worm/bec-1/bec-1-uniprot.txt
          supporting_text: GO:0031410; C:cytoplasmic vesicle; IDA:WormBase
        - reference_id: PMID:16111945
          supporting_text: Inactivation of the autophagy gene bec-1 triggers 
            apoptotic cell death in C.
  - term:
      id: GO:0006914
      label: autophagy
    evidence_type: IGI
    original_reference_id: PMID:12958363
    review:
      summary: bec-1 is required for autophagy, as demonstrated by genetic 
        interactions with other autophagy genes (unc-51/ATG1, etc.) and the 
        daf-2 insulin signaling pathway.
      action: ACCEPT
      reason: This is the core biological process for BEC-1. Strong genetic 
        evidence from the foundational autophagy study in C. elegans.
      supported_by:
        - reference_id: PMID:12958363
          supporting_text: bec-1, the C. elegans ortholog of the yeast and 
            mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal
            dauer morphogenesis and life-span extension
  - term:
      id: GO:0008340
      label: determination of adult lifespan
    evidence_type: IGI
    original_reference_id: PMID:12958363
    review:
      summary: bec-1 is required for lifespan extension in daf-2/insulin 
        signaling mutants.
      action: ACCEPT
      reason: Foundational study demonstrating autophagy requirement for insulin
        signaling-mediated longevity.
      supported_by:
        - reference_id: PMID:12958363
          supporting_text: bec-1, the C. elegans ortholog of the yeast and 
            mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal
            dauer morphogenesis and life-span extension
  - term:
      id: GO:0040024
      label: dauer larval development
    evidence_type: IGI
    original_reference_id: PMID:12958363
    review:
      summary: bec-1 is essential for normal dauer morphogenesis. RNAi knockdown
        causes abnormalities in constitutive dauer formation in daf-2 mutants.
      action: ACCEPT
      reason: Well-documented role of bec-1 in dauer development, which requires
        autophagy for proper morphogenesis and survival.
      supported_by:
        - reference_id: PMID:12958363
          supporting_text: bec-1, the C. elegans ortholog of the yeast and 
            mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal
            dauer morphogenesis
references:
  - id: GO_REF:0000033
    title: Annotation inferences using phylogenetic trees
    findings:
      - statement: IBA annotations based on PANTHER phylogenetic trees inferring
          function from characterized orthologs
  - id: GO_REF:0000043
    title: Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword 
      mapping
    findings: []
  - id: GO_REF:0000044
    title: Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular 
      Location vocabulary mapping
    findings: []
  - id: GO_REF:0000120
    title: Combined Automated Annotation using Multiple IEA Methods
    findings: []
  - id: PMID:12958363
    title: Autophagy genes are essential for dauer development and life-span 
      extension in C. elegans.
    findings:
      - statement: BEC-1 is required for autophagy, dauer morphogenesis, and 
          lifespan extension
        supporting_text: bec-1, the C. elegans ortholog of the yeast and 
          mammalian autophagy gene APG6/VPS30/beclin1, is essential for normal 
          dauer morphogenesis and life-span extension
      - statement: Foundational paper establishing autophagy requirement in C. 
          elegans longevity
        supporting_text: Dauer formation is associated with increased autophagy 
          and also requires C. elegans orthologs of the yeast autophagy genes 
          APG1, APG7, APG8, and AUT10
  - id: PMID:16111945
    title: Inactivation of the autophagy gene bec-1 triggers apoptotic cell 
      death in C. elegans.
    findings:
      - statement: BEC-1 is essential for development and necessary for 
          VPS-34/LET-512 function
        supporting_text: BEC-1, the C. elegans ortholog of the yeast and 
          mammalian autophagy proteins Atg6/Vps30 and Beclin 1, is essential for
          development
      - statement: BEC-1 forms a complex with CED-9/BCL-2 and regulates 
          apoptosis
        supporting_text: BEC-1 forms a complex with the antiapoptotic protein 
          CED-9/Bcl-2, and its depletion triggers CED-3/Caspase-dependent PCD
  - id: PMID:17172799
    title: Autophagy genes protect against disease caused by polyglutamine 
      expansion proteins in Caenorhabditis elegans.
    findings:
      - statement: Autophagy genes including bec-1 protect against polyQ 
          toxicity
        supporting_text: genetic inactivation of autophagy genes accelerates the
          accumulation of polyQ40 aggregates in C. elegans muscle cells
  - id: PMID:17327275
    title: Influence of autophagy genes on ion-channel-dependent neuronal 
      degeneration in Caenorhabditis elegans.
    findings:
      - statement: bec-1 contributes to ion-channel-dependent neurotoxicity
        supporting_text: Inactivation of unc-51, bec-1 and lgg-1, the worm 
          counterparts of the yeast autophagy genes Atg1, Atg6 and Atg8 
          respectively, partially suppresses degeneration of neurons with toxic 
          ion channel variants
  - id: PMID:17785524
    title: Dual roles of autophagy in the survival of Caenorhabditis elegans 
      during starvation.
    findings:
      - statement: Physiological autophagy promotes starvation survival
        supporting_text: we show that physiological levels of autophagy act to 
          promote survival in Caenorhabditis elegans during starvation
  - id: PMID:17890369
    title: Autophagy genes unc-51 and bec-1 are required for normal cell size in
      Caenorhabditis elegans.
    findings:
      - statement: bec-1 mutants have small body size
        supporting_text: mutational inactivation of two autophagy genes 
          unc-51/atg1 and bec-1/atg6/beclin1 results in small body size without 
          affecting cell number
  - id: PMID:17912023
    title: Autophagy is required for dietary restriction-mediated life span 
      extension in C. elegans.
    findings:
      - statement: bec-1 is required for dietary restriction longevity in eat-2 
          mutants
        supporting_text: two essential autophagy genes (bec-1 and Ce-atg7) are 
          required for the longevity phenotype of the C. elegans dietary 
          restriction mutant
  - id: PMID:21116129
    title: The coiled-coil domain protein EPG-8 plays an essential role in the 
      autophagy pathway in C. elegans.
    findings:
      - statement: EPG-8 directly interacts with BEC-1
        supporting_text: EPG-8 directly interacts with the C. elegans Beclin 1 
          homolog, BEC-1
      - statement: EPG-8 functions as C. elegans ATG14 homolog
        supporting_text: Our study demonstrates that epg-8 may function as a 
          highly divergent homolog of the yeast autophagy gene Atg14
  - id: PMID:21183797
    title: The Atg6/Vps30/Beclin 1 ortholog BEC-1 mediates endocytic retrograde 
      transport in addition to autophagy in C. elegans.
    findings:
      - statement: BEC-1 functions in endosome-to-Golgi retrograde transport
        supporting_text: we report that BEC-1, the C. elegans ortholog of 
          Atg6/Vps30/Beclin1, a key regulator of the autophagic machinery, also 
          contributes to endosome function
      - statement: BEC-1 is required for apoptotic corpse clearance
        supporting_text: We further identify a requirement for BEC-1 in the 
          clearance of apoptotic corpses in the hermaphrodite gonad, suggesting 
          a role for BEC-1 in phagosome maturation
  - id: PMID:21906946
    title: Autophagy and lipid metabolism coordinately modulate life span in 
      germline-less C. elegans.
    findings:
      - statement: Autophagy required for germline-less longevity
        supporting_text: Germline removal extends life span in C. elegans via 
          genes such as the lipase LIPL-4
  - id: PMID:26783301
    title: Negative regulation of phosphatidylinositol 3-phosphate levels in 
      early-to-late endosome conversion.
    findings:
      - statement: BEC-1 is part of the PI3K complex that generates PtdIns3P
        supporting_text: SORF-1 and SORF-2 act in a complex with BEC-1/Beclin1
      - statement: SORF-1 and SORF-2 interact with BEC-1 to regulate PI3K 
          activity
        supporting_text: Loss of sorf-1 or sorf-2 leads to greatly elevated 
          endosomal PtdIns3P, which drives excessive fusion of early endosomes
  - id: PMID:28285998
    title: A Non-Cell-Autonomous Role of BEC-1/BECN1/Beclin1 in Coordinating 
      Cell-Cycle Progression and Stem Cell Proliferation during Germline 
      Development.
    findings:
      - statement: BEC-1 required for germline stem cell proliferation
        supporting_text: We found that autophagy genes such as 
          bec-1/BECN1/Beclin1, atg-16.2/ATG16L, atg-18/WIPI1/2, and atg-7/ATG7 
          are required for the late larval expansion of germline stem cell 
          progenitors
      - statement: Acts non-cell-autonomously
        supporting_text: we report that BEC-1/BECN1/Beclin1 functions 
          non-cell-autonomously to facilitate cell-cycle progression and stem 
          cell proliferation
  - id: file:worm/bec-1/bec-1-deep-research-falcon.md
    title: Deep research on bec-1 gene function
    findings:
      - statement: BEC-1 functions as scaffold/adaptor for PI3KC3 complexes
        supporting_text: BEC-1 functions primarily as a scaffold/adaptor for 
          class III PI3K complexes (VPS-34 with VPS-15)
core_functions:
  - molecular_function:
      id: GO:0030674
      label: protein-macromolecule adaptor activity
    description: BEC-1 functions as a scaffold/adaptor within class III PI3K 
      complexes, bridging the VPS-34 catalytic kinase with complex-specific 
      subunits (EPG-8/ATG14 for autophagy, UVRAG for endocytosis) and regulatory
      proteins (SORF-1/2, CED-9).
  - molecular_function:
      id: GO:0043548
      label: phosphatidylinositol 3-kinase binding
    description: BEC-1 directly binds VPS-34, the class III PI3K catalytic 
      subunit, enabling PtdIns3P production required for autophagy initiation 
      and endosomal trafficking.
  - molecular_function:
      id: GO:0030674
      label: protein-macromolecule adaptor activity
    description: BEC-1 is essential for autophagosome nucleation as part of the 
      PI3KC3-C1 complex, generating PtdIns3P at phagophore assembly sites.
    directly_involved_in:
      - id: GO:0000045
        label: autophagosome assembly
    in_complex:
      id: GO:0034271
      label: phosphatidylinositol 3-kinase complex, class III, type I
  - molecular_function:
      id: GO:0030674
      label: protein-macromolecule adaptor activity
    description: BEC-1 functions in endocytic trafficking through the PI3KC3-C2 
      complex, regulating endosome maturation and retrograde transport.
    directly_involved_in:
      - id: GO:0006897
        label: endocytosis
    in_complex:
      id: GO:0034272
      label: phosphatidylinositol 3-kinase complex, class III, type II
proposed_new_terms: []
suggested_questions:
  - question: Does BEC-1 have distinct pools for autophagy versus endocytosis 
      functions?
  - question: What regulates the balance between PI3KC3-C1 and PI3KC3-C2 complex
      formation?
  - question: Is the nuclear localization of BEC-1 functionally significant?
suggested_experiments:
  - description: Tissue-specific rescue experiments to determine which tissues 
      require BEC-1 for different phenotypes
  - description: Structure-function analysis to identify domains required for 
      different protein interactions
  - description: Live imaging of BEC-1 dynamics during autophagy induction 
      versus endosome maturation
tags:
  - caeel-proteostasis
  - caeel-mitophagy