期刊
MOLECULAR AND CELLULAR BIOLOGY
卷 26, 期 6, 页码 2273-2285出版社
AMER SOC MICROBIOLOGY
DOI: 10.1128/MCB.26.6.2273-2285.2006
关键词
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HuD is an RNA-binding protein that has been shown to induce neuronal differentiation by stabilizing labile mRNAs carrying AU-rich instability elements. Here, we show a novel mechanism of arginine methylation of HuD by coactivator-associated arginine methyltransferase 1 (CARM1) that affected mRNA turnover of p21(cip1/waf1) mRNA in PC12 cells. CARM1 specifically methylated HuD in vitro and in vivo and colocalized with HuD in the cytoplasm. Inhibition of HuD methylation by CARM1 knockdown elongated the p21(cip1/waf1) mRNA half-life and resulted in a slow growth rate and robust neuritogenesis in response to nerve growth factor (NGF). Methylation-resistant HuD bound more p21(cip1/waf1) mRNA than did the wild type, and its overexpression upregulated p21(cip1/waf1) protein expression. These results suggested that CARM1-methylated HuD maintains PC12 cells in the proliferative state by committing p21(cip1/waf1) mRNA to its decay system. Since the methylated population of HuD was reduced in NGF-treated PC12 cells, downregulation of HuD methylation is a possible pathway through which NGF induces differentiation of PC12 cells.
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