| RRC ID |
67115
|
| Author |
Zhao YF, He XX, Song ZF, Guo Y, Zhang YN, Yu HL, He ZX, Xiong WC, Guo W, Zhu XJ.
|
| Title |
Human antigen R-regulated mRNA metabolism promotes the cell motility of migrating mouse neurons.
|
| Journal |
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.
|
| Volume |
147(6)
|
| Published |
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
|
| Resource |
| DNA material |
Genome Network Project Human cDNA Clone IRAK014I22 (HGX005814) |
