NDLI: Chx10 is required to block photoreceptor differentiation but is dispensable for progenitor proliferation in the postnatal retina

Content Provider	PubMed Central
Author	Livne-bar, Izzy Pacal, Marek Cheung, Melissa C. Hankin, Mark Judy, Trogadis Chen, Danian Dorval, Kimberley M. Bremner, Rod
Copyright Year	2006
Abstract	In the Chx10-null ocular retardation (orJ) mouse, retinal progenitor cell (RPC) proliferation is impaired, and bipolar neurons, a late born cell type, fail to differentiate. It is unclear whether Chx10 is required to maintain proliferation throughout retinogenesis or whether the bipolar cell defect is an indirect effect of growth arrest. We show that Chx10 is dispensable for late-stage RPC proliferation but is essential to promote bipolar cell genesis in place of rods. Ectopic Chx10 expression drove bipolar instead of rod cell differentiation without affecting division. Converting Chx10 to an activator impaired bipolar cell differentiation, implying that repression is important for Chx10 activity. In the Chx10 null orJ retina, only a small fraction of cells expressing mutated Chx10 mRNA were rods, but this fraction increased after p27Kip1 inactivation, which partially rescues proliferation. Most significantly, acute Chx10 knockdown in the postnatal retina promoted rods in place of bipolar neurons without affecting division. Thus, Chx10 directly controls bipolar cell genesis by inhibiting rod differentiation independent of its temporally limited early effect on RPC proliferation.
Related Links	http://dx.doi.org/10.1073/pnas.0600083103
Starting Page	4988
File Format	PDF
ISSN	10916490
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	13
Volume Number	103
Language	English
Publisher	National Academy of Sciences
Publisher Date	2006-03-28
Access Restriction	Open
Rights Holder	National Academy of Sciences
Subject Keyword	Research in Higher Education
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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