SCYL1 arginine methylation by PRMT1 is essential for neurite outgrowth via Golgi morphogenesis
Genki Amano, Shinsuke Matsuzaki, Yasutake Mori, Ko Miyoshi, Sarina Han, Sho Shikada, Hironori Takamura, Takeshi Yoshimura, Taiichi Katayama
Abstract
-COP. PRMT1 was colocalized with SCYL1 in the Golgi fraction. Inhibition of PRMT1 suppressed axon outgrowth and dendrite complexity via abnormal Golgi morphology. Knockdown of SCYL1 by small interfering RNA (siRNA) inhibited axon outgrowth, and the inhibitory effect was rescued by siRNA-resistant SCYL1, but not SCYL1 mutant, in which the arginine methylation site was replaced. Thus, PRMT1 regulates Golgi morphogenesis via SCYL1 arginine methylation. We propose that SCYL1 arginine methylation by PRMT1 contributes to axon and dendrite morphogenesis in neurons.
Topics & Concepts
BiologyNeuriteGolgi apparatusMorphogenesisCell biologyMethylationArginineGeneticsGeneEndoplasmic reticulumIn vitroAmino acidCancer-related gene regulationEpigenetics and DNA Methylation