RRC ID 67115
著者 Zhao YF, He XX, Song ZF, Guo Y, Zhang YN, Yu HL, He ZX, Xiong WC, Guo W, Zhu XJ.
タイトル Human antigen R-regulated mRNA metabolism promotes the cell motility of migrating mouse neurons.
ジャーナル Development
Abstract Neocortex development during embryonic stages requires the precise control of mRNA metabolism. Human antigen R (HuR) is a well-studied mRNA-binding protein that regulates mRNA metabolism, and it is highly expressed in the neocortex during developmental stages. Deletion of HuR does not impair neural progenitor cell proliferation or differentiation, but it disturbs the laminar structure of the neocortex. We report that HuR is expressed in postmitotic projection neurons during mouse brain development. Specifically, depletion of HuR in these neurons led to a mislocalization of CDP+ neurons in deeper layers of the cortex. Time-lapse microscopy showed that HuR was required for the promotion of cell motility in migrating neurons. PCR array identified profilin 1 (Pfn1) mRNA as a major binding partner of HuR in neurons. HuR positively mediated the stability of Pfn1 mRNA and influenced actin polymerization. Overexpression of Pfn1 successfully rescued the migration defects of HuR-deleted neurons. Our data reveal a post-transcriptional mechanism that maintains actin dynamics during neuronal migration.
巻・号 147(6)
公開日 2020-3-16
DOI 10.1242/dev.183509
PII dev.183509
PMID 32098764
PMC PMC7097226
MeSH Animals Body Patterning / genetics Cell Movement* / genetics Cells, Cultured ELAV-Like Protein 1 / physiology* Embryo, Mammalian Female HEK293 Cells Humans Male Mice Mice, Inbred C57BL Mice, Transgenic Neural Stem Cells / physiology Neurogenesis / genetics Neurons / physiology* Pregnancy Profilins / physiology RNA Processing, Post-Transcriptional / genetics RNA, Messenger / metabolism*
IF 5.611
リソース情報
遺伝子材料 Genome Network Project Human cDNA Clone IRAK014I22 (HGX005814)