Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot keyword mapping
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping
Electronic Gene Ontology annotations created by ARBA machine learning models
Combined Automated Annotation using Multiple IEA Methods
C. elegans dynamin-related protein DRP-1 controls severing of the mitochondrial outer membrane.
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Established DRP-1 as the mitochondrial fission factor in C. elegans
"wild-type DRP-1 contributes to the final stages of mitochondrial division by controlling scission of the mitochondrial outer membrane."
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Mutant DRP-1 inhibits outer membrane scission while inner membrane scission still occurs
"Mutant DRP-1 causes the mitochondrial matrix to retract into large blebs that are both surrounded and connected by tubules of outer membrane."
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DRP-1::GFP localizes to sites of mitochondrial scission
"DRP-1 fused to GFP is observed in spots on mitochondria where scission eventually occurs."
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Overexpression causes excessive mitochondrial fragmentation
"Overexpressed wild-type DRP-1 causes mitochondria to become excessively fragmented"
DRP-1-mediated mitochondrial fragmentation during EGL-1-induced cell death in C. elegans.
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DRP-1 is required and sufficient to induce mitochondrial fragmentation during apoptosis
"DRP-1/dynamin-related protein, a key component of the mitochondrial fission machinery, is required and sufficient to induce mitochondrial fragmentation and programmed cell death during C. elegans development."
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Mitochondrial fragmentation is induced by EGL-1 and blocked by ced-9 mutations
"Mitochondrial fragmentation is induced by the BH3-only protein EGL-1 and can be blocked by mutations in the bcl-2-like gene ced-9"
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Mitochondrial fragmentation is independent of CED-4 and CED-3
"Mitochondrial fragmentation is independent of CED-4/Apaf-1 and CED-3/caspase"
Caenorhabditis elegans drp-1 and fis-2 regulate distinct cell-death execution pathways downstream of ced-3 and independent of ced-9.
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drp-1 is not required for apoptosis activation but acts downstream of CED-3
"profusion genes fzo-1 and eat-3 or the profission gene drp-1 are not required for apoptosis activation in C. elegans."
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DRP-1 promotes mitochondrial elimination in dying cells
"drp-1 and fis-2 function independent of one another and the Bcl-2 homolog CED-9 and downstream of the CED-3 caspase to promote elimination of mitochondria in dying cells"
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CED-3 cleaves DRP-1; this cleavage is required for pro-apoptotic but not fission function
"CED-3 can cleave DRP-1, which appears to be important for DRP-1's proapoptotic function, but not its mitochondria fission function."
CED-9 and mitochondrial homeostasis in C. elegans muscle.
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CED-9 overexpression causes interconnected mitochondria
"increased CED-9 expression in these cells produces highly interconnected mitochondria."
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DRP-1 overexpression suppresses CED-9-induced mitochondrial connectivity
"This mitochondrial phenotype is partially suppressed by increased expression of the dynamin-related GTPase DRP-1"
Bcl-2 proteins EGL-1 and CED-9 do not regulate mitochondrial fission or fusion in Caenorhabditis elegans.
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drp-1 mutants have defective fission with normal fusion
"in a drp-1 mutant, in which mitochondrial fusion occurs but mitochondrial fission is defective"
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EGL-1 and CED-9 do not regulate mitochondrial fission or fusion
"loss of egl-1 or ced-9, or overexpression of their gene products, had no apparent effect on mitochondrial connectivity or mitochondrial size."
The dynamin-related protein DRP-1 and the insulin signaling pathway cooperate to modulate Caenorhabditis elegans longevity.
A molecular switch that governs mitochondrial fusion and fission mediated by the BCL2-like protein CED-9 of Caenorhabditis elegans.
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DRP-1 interacts with CED-9
"CED-9 also physically interacts with the mitochondrial fission protein DRP-1"
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Interaction is enhanced by GTP rather than GDP
"this interaction can be enhanced when CED-9 is associated with the BH3-only protein EGL-1."
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DRP-1 is recruited to mitochondria by CED-9/EGL-1 complex
"the EGL-1-CED-9 complex promotes mitochondrial fission by recruiting DRP-1 to mitochondria"
Autophagy facilitates mitochondrial rebuilding after acute heat stress via a DRP-1-dependent process.
Deep research summary for drp-1
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DRP-1 is recruited from cytosol to OMM by adaptor proteins including FIS-1, FIS-2 and MFF-1/MFF-2
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Loss of drp-1 in dystrophin mutants reduces TUNEL-positive muscle cells from 5.28 to 2.07 per animal
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drp-1 disruption during development extends daf-2 (IIS) mutant longevity