Cyclin D1 inactivation extends proliferation and alters histogenesis in the postnatal mouse retina
Cyclin D1 inactivation extends proliferation and alters histogenesis in the postnatal mouse retina
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DOI：
10.1002/dvdy.23782
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发表时间：
2012-05-01
影响因子：
2.5
通讯作者：
Levine, Edward M.
中科院分区：
文献类型：
--
作者：
Das, Gaurav;Clark, Anna M.;Levine, Edward M.
背景：细胞周期调节因子Cyclin D1在胚胎视网膜祖细胞（RPCs）中表达，并调节其细胞周期速率和神经源性输出。我们在这里报道了Cyclin D1在出生后视网膜组织发生中也有重要的功能。结果：在Cyclin D1敲除（Ccnd1-/-）视网膜中，Muller胶质细胞和双极细胞的初始产生增强。尽管RPC群体在胚胎时期的耗损率比正常情况下要快，但出生后的Ccnd1-/-视网膜却表现出了更长的增殖、神经发生和胶质发生窗口期。通常局限于Muller胶质细胞的Cyclin D3在Ccnd1-/- rpc中过早表达。然而，在调节细胞周期动力学或神经源性输出方面，Cyclin D3并不能补偿Cyclin D1。结论：本研究的数据以及我们之前发现的Cyclin D2不能完全补偿Cyclin D1缺失的结果表明，Cyclin D1调节视网膜组织发生的方式与其他d - Cyclin不同。科学进展(1):1 - 4,2012。(c) 2012 Wiley期刊有限公司
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 Muller 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 Muller 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. Developmental Dynamics 241:941952, 2012. (c) 2012 Wiley Periodicals, Inc.