Autism is a disorder of brain development characterized by impaired social interaction and communication. The latest child autopsy studies suggest the abnormality of neuronal fate specification during pregnancy. Copy Number Variation(CNV) in Chromosome 16p13.11 is one of known risk factors of autism. We hypothesize that one or several candidate genes in 16p.13.11 locus could be responsible for neurogenesis and pathophysiology of autism.
After expression screening by in situ hybridization in mouse developing brain, we examined the function of RNA binding protein Meiosis Arrest Female 1 (MARF1). It has been already reported that Oocyte form of MARF1 (oMARF1) suppresses the target molecules via its own RNase activity, and is indispensable for oogenic process. However, the function of another isoform, somatic form of MARF1 (sMARF1) is still obscure.
Here we report the expression pattern and function of sMARF1 in developing mouse brain. sMARF1 protein highly expresses in embryonic brain tissue and more in matured differentiated neurons than cortical pogenitors. The overexpression of sMARF1 in neuronal precursor cells which is derived from e12.5 cortices, increases the number of Tuj1-positive differentiated neurons, while the knockdown of sMARF1 increases the number of Ki67-positive proliferating cell in vitro. The knockdown of sMARF1 in vivo by in utero electroporation increases the ratio of proliferating cell in subventricular zone. These results suggest that sMARF1 regulates neuronal differentiation in developing brain.