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- W3196557353 abstract "Abstract Neuronal regeneration after injury depends on the intrinsic growth potential of neurons. Our study shows that UNC-16, a Caenorhabditis elegans JIP3 homolog, inhibits axonal regeneration by regulating initiation and rate of regrowth. This occurs through the inhibition of the regeneration-promoting activity of the long isoform of DLK-1 and independently of the inhibitory short isoform of DLK-1. We show that UNC-16 promotes DLK-1 punctate localization in a concentration-dependent manner limiting the availability of the long isoform of DLK-1 at the cut site, minutes after injury. UNC-16 negatively regulates actin dynamics through DLK-1 and microtubule dynamics partially via DLK-1. We show that post-injury cytoskeletal dynamics in unc-16 mutants are also partially dependent on CEBP-1. The faster regeneration seen in unc-16 mutants does not lead to functional recovery. Our data suggest that the inhibitory control by UNC-16 and the short isoform of DLK-1 balances the intrinsic growth-promoting function of the long isoform of DLK-1 in vivo. We propose a model where UNC-16’s inhibitory role in regeneration occurs through both a tight temporal and spatial control of DLK-1 and cytoskeletal dynamics." @default.
- W3196557353 created "2021-09-13" @default.
- W3196557353 creator A5008410104 @default.
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- W3196557353 creator A5087890604 @default.
- W3196557353 date "2021-08-28" @default.
- W3196557353 modified "2023-10-16" @default.
- W3196557353 title "UNC-16 alters DLK-1 localization and negatively regulates actin and microtubule dynamics in <i>Caenorhabditis elegans</i> regenerating neurons" @default.
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- W3196557353 doi "https://doi.org/10.1093/genetics/iyab139" @default.
- W3196557353 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/8570795" @default.
- W3196557353 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/34740241" @default.
- W3196557353 hasPublicationYear "2021" @default.