Rb regulates proliferation and rod photoreceptor development in the mouse retina

被引:146
|
作者
Zhang, JK
Gray, J
Wu, LZ
Leone, G
Rowan, S
Cepko, CL
Zhu, XM
Craft, CM
Dyer, MA
机构
[1] St Jude Childrens Res Hosp, Dept Dev Neurobiol, Memphis, TN 38105 USA
[2] Ohio State Univ, Dept Mol Genet, Columbus, OH 43210 USA
[3] Harvard Univ, Sch Med, Dept Genet, Boston, MA 02115 USA
[4] Harvard Univ, Sch Med, Howard Hughes Med Inst, Boston, MA 02115 USA
[5] Univ So Calif, Dept Cell & Neurobiol, Los Angeles, CA 90033 USA
基金
美国国家卫生研究院;
关键词
D O I
10.1038/ng1318
中图分类号
Q3 [遗传学];
学科分类号
071007 ; 090102 ;
摘要
The retinoblastoma protein (Rb) regulates proliferation, cell fate specification and differentiation in the developing central nervous system (CNS), but the role of Rb in the developing mouse retina has not been studied, because Rb-deficient embryos die before the retinas are fully formed. We combined several genetic approaches to explore the role of Rb in the mouse retina. During postnatal development, Rb is expressed in proliferating retinal progenitor cells and differentiating rod photoreceptors. In the absence of Rb, progenitor cells continue to divide, and rods do not mature. To determine whether Rb functions in these processes in a cell-autonomous manner, we used a replication-incompetent retrovirus encoding Cre recombinase to inactivate the Rb1(lox) allele in individual retinal progenitor cells in vivo. Combined with data from studies of conditional inactivation of Rb1 using a combination of Cre transgenic mouse lines, these results show that Rb is required in a cell-autonomous manner for appropriate exit from the cell cycle of retinal progenitor cells and for rod development.
引用
收藏
页码:351 / 360
页数:10
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