L. Ma and J.C. Hocking contributed equally to this study.
Zac1 promotes a Müller glial cell fate and interferes with retinal ganglion cell differentiation in Xenopus retina
Article first published online: 27 OCT 2006
Copyright © 2006 Wiley-Liss, Inc.
Volume 236, Issue 1, pages 192–202, January 2007
How to Cite
Ma, L., Hocking, J. C., Hehr, C. L., Schuurmans, C. and McFarlane, S. (2007), Zac1 promotes a Müller glial cell fate and interferes with retinal ganglion cell differentiation in Xenopus retina. Dev. Dyn., 236: 192–202. doi: 10.1002/dvdy.21002
- Issue published online: 19 DEC 2006
- Article first published online: 27 OCT 2006
- Manuscript Accepted: 1 OCT 2006
- Canadian Institutes of Health Research (CIHR). Grant Number: MOP-14138
- March of Dimes Operating Grant
- Plag family zinc finger transcription factor;
- tumor suppressor gene;
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. Developmental Dynamics 236:192–202, 2007. © 2006 Wiley-Liss, Inc.