RRC ID 59595
著者 Shimizu T, Kato Y, Sakai Y, Hisamoto N, Matsumoto K.
タイトル N-Glycosylation of the Discoidin Domain Receptor Is Required for Axon Regeneration in Caenorhabditis elegans.
ジャーナル Genetics
Abstract Axon regeneration following neuronal injury is an important repair mechanism that is not well understood at present. In Caenorhabditis elegans, axon regeneration is regulated by DDR-2, a receptor tyrosine kinase (RTK) that contains a discoidin domain and modulates the Met-like SVH-2 RTK-JNK MAP kinase signaling pathway. Here, we describe the svh-10/sqv-3 and svh-11 genes, which encode components of a conserved glycosylation pathway, and show that they modulate axon regeneration in C. elegans Overexpression of svh-2, but not of ddr-2, can suppress the axon regeneration defect observed in svh-11 mutants, suggesting that SVH-11 functions between DDR-2 and SVH-2 in this glycosylation pathway. Furthermore, we found that DDR-2 is N-glycosylated at the Asn-141 residue located in its discoidin domain, and mutation of this residue caused an axon regeneration defect. These findings indicate that N-linked glycosylation plays an important role in axon regeneration in C. elegans.
巻・号 213(2)
ページ 491-500
公開日 2019-10-1
DOI 10.1534/genetics.119.302492
PII genetics.119.302492
PMID 31371405
PMC PMC6781908
MeSH Animals Axons / metabolism Axons / physiology Caenorhabditis elegans / genetics Caenorhabditis elegans / growth & development Caenorhabditis elegans Proteins / genetics* Discoidin Domain Receptor 2 / genetics* Discoidin Domain Receptors / genetics Fucosyltransferases / genetics* Glycosylation MAP Kinase Signaling System / genetics Mutation Nerve Regeneration / genetics* Neurons / metabolism Receptor Protein-Tyrosine Kinases / genetics*
IF 3.564
引用数 0
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線虫 tm797