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

• DOI: 10.1073/pnas.0600083103
• Publication Date: 2006-03-18T01:34:25Z
• Authors: Izzy Livne-bar; Marek Pacal; Melissa C. Cheung; Mark Hankin; Judy Trogadis; Danian Chen; Kimberley M. Dorval; Rod Bremner
• Keywords: Homeodomain Proteins; Mice, Knockout; 0301 basic medicine; Stem Cells; Cell Polarity; Cell Differentiation; Rats; Mice; 03 medical and health sciences; Animals, Newborn; Animals; Photoreceptor Cells; RNA, Messenger; Cell Proliferation; Transcription Factors

In the Chx10 -null ocular retardation (or J ) mouse, retinal progenitor cell (RPC) proliferation is impaired, and bipolar neurons, a late born type, fail to differentiate. It unclear whether required maintain throughout retinogenesis or defect an indirect effect of growth arrest. We show that dispensable for late-stage RPC but essential promote genesis in place rods. Ectopic expression drove instead rod differentiation without affecting division. Converting activator impaired differentiation, implying repression important activity. null retina, only small fraction cells expressing mutated mRNA were rods, this increased after p27 Kip1 inactivation, which partially rescues proliferation. Most significantly, acute knockdown postnatal retina promoted rods neurons Thus, directly controls by inhibiting independent its temporally limited early on