Sharma Kedarlal, Singh Juhi, Frost Emma E, Pillai Prakash P
Division of Neurobiology, Department of Zoology, Faculty of Science, The M. S. University of Baroda, Gujarat, India;
Division of Neurobiology, Department of Zoology, Faculty of Science, The M. S. University of Baroda, Gujarat, India.
Acta Neurobiol Exp (Wars). 2018;78(1):30-40.
avMethyl‑CpG binding protein 2 (MeCP2) is an epigenetic regulator, which preferentially binds to methylated CpG dinucleotides in DNA. MeCP2 mutations have been linked to Rett syndrome, a neurodevelopmental disorder characterized by severe intellectual disability in females. Earlier studies indicated that loss of MeCP2 function in neuronal cells was the sole cause of Rett syndrome. Subsequent studies have linked MeCP2 expression in CNS glial cells to Rett syndrome pathogenesis. In this review, we have discussed the role of MeCP2 in glial subtypes, astrocytes, oligodendrocytes and microglia, and how loss of MeCP2 function in these cells has a profound influence on both glial and neuronal function.
甲基化CpG结合蛋白2(MeCP2)是一种表观遗传调节因子,它优先结合DNA中的甲基化CpG二核苷酸。MeCP2突变与雷特综合征有关,雷特综合征是一种神经发育障碍,其特征是女性严重智力残疾。早期研究表明,神经元细胞中MeCP2功能的丧失是雷特综合征的唯一原因。随后的研究将中枢神经系统神经胶质细胞中MeCP2的表达与雷特综合征的发病机制联系起来。在这篇综述中,我们讨论了MeCP2在神经胶质细胞亚型、星形胶质细胞、少突胶质细胞和小胶质细胞中的作用,以及这些细胞中MeCP2功能的丧失如何对神经胶质细胞和神经元功能产生深远影响。