Abnormal expression and dysfunction of methyl-CpG binding protein 2 （MeCP2） cause Rett syndrome （RTT）. The diverse phosphorylation modifications modulate MeCP2 function in neural cells. Using western blot and immu...Abnormal expression and dysfunction of methyl-CpG binding protein 2 （MeCP2） cause Rett syndrome （RTT）. The diverse phosphorylation modifications modulate MeCP2 function in neural cells. Using western blot and immunohistochemistry, we examined the expression patterns of MeCP2 and three phospho-MeCP2s （pMeCP2s） in the developing rat brain. The expression of MeCP2 and phospho-S80 （pS80） MeCP2 increased while pS421 MeCP2 and pS292 MeCP2 decreased with brain maturation. In contrast to the nuclear localization of MeCP2 and pS80 MeCP2, pS421 MeCP2 and pS292 MeCP2 were mainly expressed in the cytoplasmic com- partment. Apart from their distribution in neurons, they were also detected at a low level in astrocytes. Postnatallyinitiated MeCP2 deficiency affected cerebellar neural cell development, as determined by the abnormal expression of GFAP, DCX, Tuj 1, MAP-2, and calbindin-D28k. Together, these results demonstrate that MeCP2 and diverse pMeCP2s have distinct features of spatio-temporal expression in the rat brain, and that the precise levels of MeCP2 in the postnatal period are vital to cerebellar neural cell development.展开更多
基金supported by a grant from the National Natural Science Foundation of China(81030020)
文摘Abnormal expression and dysfunction of methyl-CpG binding protein 2 （MeCP2） cause Rett syndrome （RTT）. The diverse phosphorylation modifications modulate MeCP2 function in neural cells. Using western blot and immunohistochemistry, we examined the expression patterns of MeCP2 and three phospho-MeCP2s （pMeCP2s） in the developing rat brain. The expression of MeCP2 and phospho-S80 （pS80） MeCP2 increased while pS421 MeCP2 and pS292 MeCP2 decreased with brain maturation. In contrast to the nuclear localization of MeCP2 and pS80 MeCP2, pS421 MeCP2 and pS292 MeCP2 were mainly expressed in the cytoplasmic com- partment. Apart from their distribution in neurons, they were also detected at a low level in astrocytes. Postnatallyinitiated MeCP2 deficiency affected cerebellar neural cell development, as determined by the abnormal expression of GFAP, DCX, Tuj 1, MAP-2, and calbindin-D28k. Together, these results demonstrate that MeCP2 and diverse pMeCP2s have distinct features of spatio-temporal expression in the rat brain, and that the precise levels of MeCP2 in the postnatal period are vital to cerebellar neural cell development.
