Gene Ontology annotation through association of InterPro records with GO terms
Annotation inferences using phylogenetic trees
Gene Ontology annotation based on UniProtKB/Swiss-Prot Subcellular Location vocabulary mapping, accompanied by conservative changes to GO terms applied by UniProt
Receptor-mediated endocytosis in the Caenorhabditis elegans oocyte.
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mu2 RNAi does not reduce yolk uptake into oocytes, unlike clathrin, alpha- and beta-adaptin RNAi.
"Unlike the other CCP components we tested, Ce- μ2(RNAi) and Ce- ς2(RNAi) did not result in an apparent reduction in YP170::GFP uptake into the oocyte."
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mu2 RNAi progeny are severely dumpy.
"All progeny of Ce- μ2(RNAi) and Ce- ς2(RNAi) mothers were severely dumpy (Dpy)."
C. elegans AP-2 and retromer control Wnt signaling by regulating mig-14/Wntless.
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dpy-23 mutants display Wnt-pathway phenotypes and DPY-23 acts in Wnt-producing cells.
"DPY-23 acts in Wnt-expressing cells to promote these processes."
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MIG-14/Wntless accumulates at the plasma membrane in dpy-23 mutants.
"In dpy-23 mutants, MIG-14 accumulates at or near the plasma membrane."
Mu2 adaptin facilitates but is not essential for synaptic vesicle recycling in Caenorhabditis elegans.
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dpy-23/apm-2 encodes the only mu2 subunit of AP-2 in C. elegans.
"Here, we characterize the apm-2 gene (also called dpy-23), which encodes the only micro2 subunit in the nematode Caenorhabditis elegans."
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APM-2::GFP localises to synapses with synaptobrevin and clathrin heavy chain.
"APM-2∷GFP is localized at synapses and colocalizes with the synaptic vesicle protein synaptobrevin/VAMP"
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Loss of mu2 mislocalises synaptic clathrin and reduces vesicle number and evoked release to ~60%, but vesicles are still recycled.
"In apm-2 mutants, clathrin is mislocalized at synapses, and synaptic vesicle numbers and evoked responses are reduced to 60 and 65%, respectively."
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Mu2 stabilises the AP-2 complex; alpha adaptin falls to 60% (e840) and 12% (gm17).
"The reduction in α adaptin levels in both alleles indicates that μ2 is required to stabilize the AP2 complex; however, some residual α adaptin remains in the absence of μ2."
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Yolk uptake persists in apm-2 nulls.
"Over 98% of the gonads in both apm-2(e840) and apm-2(gm17) mutants were scored as positive for yolk protein uptake"
Endocytosis and intracellular trafficking contribute to necrotic neurodegeneration in C. elegans.
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Endocytosis is required for execution of necrotic neurodegeneration; the abstract names dynamin, synaptotagmin and endophilin.
"Depletion of the key endocytic machinery components dynamin, synaptotagmin and endophilin suppresses necrotic neurodegeneration induced by diverse genetic and environmental insults in C. elegans."
Endocytosis genes facilitate protein and membrane transport in C. elegans sensory cilia.
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AP-2 localises to a periciliary membrane compartment and endocytic mutants show expanded ciliary membranes and ciliary protein mislocalisation.
"Disruption of endocytic gene function causes expansion of ciliary and/or periciliary membranes as well as defects in the ciliary targeting and/or transport dynamics of ciliary transmembrane and IFT proteins."
Clathrin and AP2 are required for phagocytic receptor-mediated apoptotic cell clearance in Caenorhabditis elegans.
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RNAi of dpy-23 increases germ-cell corpses in the ced-1/ced-6 pathway.
"A time-course analysis confirmed that germ cell corpses increased significantly in an age-dependent manner in animals with RNAi of apa-2, apb-1, and dpy-23, but not aps-2"
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DPY-23 binds CED-6 directly and co-immunoprecipitates with CED-6 in vivo.
"GST-CED-6 directly interacted with 35S-labeled APA-2, APB-1 and DPY-23, and His6-tagged CHC-1C (Figure 4A)."
The membrane-associated proteins FCHo and SGIP are allosteric activators of the AP2 clathrin adaptor complex.
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apm-2 mutants share the pleiotropic AP-2 loss phenotype and suppressors of fcho-1 map to all four AP-2 subunits.
"A subsequent screen for bypass suppressors of fcho-1 nulls identified 71 compensatory mutations in all four AP2 subunits."
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YxxPhi cargo motifs bind mu2 and are required for AP-2-mediated internalisation.
"Tyrosine motifs comprised of YxxΦ, where x is any amino acid, and Φ is a large hydrophobic residue, bind the mu2 subunit of AP2 and are required for AP2-mediated internalization"
The Caenorhabditis elegans Tubby homolog dynamically modulates olfactory cilia membrane morphogenesis and phospholipid composition.
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DPY-23::GFP is enriched at the AWB periciliary membrane compartment.
"In wild-type animals, a DPY-23::GFP AP-2 μ2 subunit fusion protein was enriched at the PCMC of AWB in a domain similar to that occupied by TUB-1"
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dpy-23 mutants have an expanded AWB ciliary membrane that is suppressed by tub-1 loss.
"As in odr-1 mutants, loss of tub-1 fully suppressed the expanded ciliary membrane phenotype of dpy-23 mutants (Figure 7C)"
Deep research report (falcon/Edison) on C. elegans dpy-23
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Deep research corroborates the mu2 cargo-adaptor model and adds GLR-1 trafficking, NEKL-kinase and SEL-5/AAK1 phosphorylation findings not in GOA.
"DPY-23/AP-2 facilitates clathrin-dependent synaptic-vesicle recycling but is not absolutely essential; residual AP-2 or alternative recycling routes likely remain."
WormBase gene description for dpy-23 (worm)