Open AccessHuman antigen R-regulated mRNA metabolism promotes the cell motility of migrating neurons
Author(s) -
Yifei Zhao,
Xiaomin He,
Zi-Fei Song,
Yifeng Guo,
Yanning Zhang,
Huali Yu,
Zixuan He,
WenCheng Xiong,
Weixiang Guo,
Xinen Zhu
Publication year - 2020
Publication title -
development
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.15
H-Index - 36
eISSN - 1477-9129
pISSN - 0950-1991
DOI - 10.1242/dev.183509
Subject(s) - neocortex , biology , microbiology and biotechnology , messenger rna , motility , rna binding protein , cell migration , in situ hybridization , corticogenesis , progenitor cell , cell , neuroscience , stem cell , genetics , gene
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.