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
Ubiquitination is required for the initial removal of paternal organelles in C. elegans.
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Demonstrated two redundant mechanisms for paternal mitochondria elimination
"Thus, there are two redundant, but temporally distinct mechanisms that target paternal mitochondria for elimination in C. elegans.
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fndc-1 provides a temporally distinct, ubiquitin-independent mechanism
"If paternal mitochondria are not eliminated via this early process, they are eventually removed from the embryo in a process that depends on the mitophagy adaptor protein, fndc-1.
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If early ubiquitin-dependent elimination fails, fndc-1-dependent mitophagy removes paternal mitochondria
"If paternal mitochondria are not eliminated via this early process, they are eventually removed from the embryo in a process that depends on the mitophagy adaptor protein, fndc-1.
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Fndc-1 contributes to paternal mitochondria elimination in C. elegans.
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FNDC-1 is expressed in sperm but not oocytes
"FNDC-1 is strongly expressed in sperm but not oocytes and contributes to paternal mitochondria elimination.
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FNDC-1 contributes to paternal mitochondria elimination
"loss of fndc-1 retards the rate of paternal mitochondria degradation, but not that of membranous organelles, a nematode specific membrane compartment whose fusion is required for sperm motility.
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Loss of fndc-1 retards paternal mitochondria degradation
"loss of fndc-1 retards the rate of paternal mitochondria degradation
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Paternal mtDNA detectable in fndc-1 mutant cross-progeny
"Paternal mitochondrial DNA is normally undetectable in wildtype larva, but can be detected in the cross-progeny of fndc-1 mutant males.
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First ubiquitin-independent mitophagy receptor identified for sperm mitochondria degradation
"This is the first example of a ubiquitin-independent mitophagy receptor playing a role in the selective degradation of sperm mitochondria.
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FNDC-1-mediated mitophagy and ATFS-1 coordinate to protect against hypoxia-reoxygenation.
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FNDC-1 is the C. elegans ortholog of FUNDC1 and mediates mitophagy under hypoxia-reoxygenation stress
"FUNDC1 (FUN14 domain containing 1) is a mammalian mitophagy receptor that responds to hypoxia-reoxygenation (HR) stress. Here, we provide evidence that FNDC-1 is the C. elegans ortholog of FUNDC1, and that its loss protects against injury in a worm model of HR.
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Loss of fndc-1 provides protection that depends on ATFS-1 and UPRmt
"This protection depends upon ATFS-1, a transcription factor that is central to the mitochondrial unfolded protein response (UPRmt).
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FNDC-1 has a role in non-hypoxic mitochondrial quality control
"These data support a role for FNDC-1 in non-hypoxic MQC, and further suggest that these changes are prophylactic in relation to subsequent HR.
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Deep research report on fndc-1