Human antigen R-regulated mRNA metabolism promotes the cell motility of migrating mouse neurons.
Yi-Fei ZhaoXiao-Xiao HeZi-Fei SongYe GuoYan-Ning ZhangHua-Li YuZi-Xuan HeWen-Cheng XiongWeixiang GuoXiao-Juan ZhuPublished in: Development (Cambridge, England) (2020)
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.
Keyphrases
- binding protein
- spinal cord
- endothelial cells
- single cell
- stem cells
- high resolution
- high throughput
- cell therapy
- cell proliferation
- machine learning
- magnetic resonance
- biofilm formation
- mesenchymal stem cells
- escherichia coli
- induced pluripotent stem cells
- high speed
- staphylococcus aureus
- genome wide
- mass spectrometry
- cystic fibrosis
- optical coherence tomography
- hiv testing