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Dev Dyn. 2012 May;241(5):941-52. doi: 10.1002/dvdy.23782.

Cyclin D1 inactivation extends proliferation and alters histogenesis in the postnatal mouse retina.

Author information

1
Departments of Ophthalmology and Visual Sciences, and Neurobiology and Anatomy, John A. Moran Eye Center, University of Utah, Salt Lake City, UT, USA.

Abstract

BACKGROUND:

The cell-cycle regulator Cyclin D1 is expressed in embryonic retinal progenitor cells (RPCs) and regulates their cell-cycle rate and neurogenic output. We report here that Cyclin D1 also has important functions in postnatal retinal histogenesis.

RESULTS:

The initial production of Müller glia and bipolar cells was enhanced in Cyclin D1 knockout (Ccnd1(-/-) ) retinas. Despite a steeper than normal rate of depletion of the RPC population at embryonic ages, postnatal Ccnd1(-/-) retinas exhibited an extended window of proliferation, neurogenesis, and gliogenesis. Cyclin D3, normally confined to Müller glia, was prematurely expressed in Ccnd1(-/-) RPCs. However, Cyclin D3 did not compensate for Cyclin D1 in regulating cell-cycle kinetics or neurogenic output.

CONCLUSIONS:

The data presented in this study along with our previous finding that Cyclin D2 was unable to completely compensate for the absence of Cyclin D1 indicate that Cyclin D1 regulates retinal histogenesis in ways not shared by the other D-cyclins.

PMID:
22434780
PMCID:
PMC3361900
DOI:
10.1002/dvdy.23782
[Indexed for MEDLINE]
Free PMC Article
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