bec-1

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. Proposed replacements: protein-macromolecule adaptor activity 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. Proposed replacements: early endosome to late endosome transport 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. Proposed replacements: early endosome to late endosome transport 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. Proposed replacements: protein-macromolecule adaptor activity 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

Gene Description

Existing Annotations Review

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).

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

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

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

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