PRMT1 and Btg2 regulates neurite outgrowth of Neuro2a cells.

摘要

Neurite outgrowth is one of the crucial events in the formation of neural circuits. The majority of studies on neurite outgrowth have focused on signal transduction processes based on phosphorylation and acetylation; a few studies have suggested the involvement of other molecular mechanisms. Recent progress in understanding the nature of protein arginine N-methyltransferases (PRMTs) raises the possibility of the involvement of protein methylation accompanied by cell shape changes during neuronal differentiation. Here, we show that PRMT1 play a pivotal role in the neurite outgrowth of Neuro2a cells. Our results revealed that PRMT1 depletion specifically affected neurite outgrowth but not the physiological processes involved in cell growth and differentiation. Furthermore, we demonstrated that Btg2, one of the PRMT1 binding partner, depletion down-regulated arginine methylation in the nucleus and inhibited neurite outgrowth. These results indicate that protein arginine methylation by PRMT1 in the nucleusis an important step in neuritogenesis.