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XB-ART-34781
Dev Dyn January 1, 2007; 236 (1): 192-202.

Zac1 promotes a Müller glial cell fate and interferes with retinal ganglion cell differentiation in Xenopus retina.

Ma L , Hocking JC , Hehr CL , Schuurmans C , McFarlane S .


Abstract
The timing of cell cycle exit is tightly linked to cell fate specification in the developing retina. Accordingly, several tumor suppressor genes, which are key regulators of cell cycle exit in cancer cells, play critical roles in retinogenesis. Here we investigated the role of Zac1, a tumor suppressor gene encoding a zinc finger transcription factor, in retinal development. Strikingly, in gain-of-function assays in Xenopus, mouse Zac1 promotes proliferation and apoptosis at an intermediate stage of retinogenesis. Zac1 also influences cell fate decisions, preferentially promoting the differentiation of tumor-like clusters of abnormal neuronal cells in the ganglion cell layer, as well as inducing the formation of supernumerary Müller glial cells at the expense of other cell types. Thus Zac1 has the capacity to influence cell cycle exit, and cell fate specification and differentiation decisions by retinal progenitors, suggesting that further functional studies will uncover new insights into how retinogenesis is regulated.

PubMed ID: 17072860
Article link: Dev Dyn

Genes referenced: casp3.2 isl1 kcnd2 myc ncam1 nefh nefl nefm plag1
Antibodies: BrdU Ab3 Casp3 Ab4 GABA Ab2 Isl1/2 Ab1 Kcnd2 Ab2 Myc Ab3 Nefm Ab2 Neuronal Ab1 Neuronal Ab5


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