Extrinsic and intrinsic factors control the genesis of amacrine and cone cells in the rat retina.
Extrinsic and intrinsic factors control the genesis of amacrine and cone cells in the rat retina.
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发表时间：
1999-02
期刊：
影响因子：
4.6
通讯作者：
Michel J. Belliveau;C. Cepko
中科院分区：
文献类型：
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作者：
Michel J. Belliveau;C. Cepko
脊椎动物神经视网膜的七大类细胞是由一群多能祖细胞产生的。最近的研究提出了一种视网膜发育模型，其中祖细胞和环境都随着时间的推移而变化(Cepko, c.l ., Austin, c.p, Yang， X., Alexiades， M.和Ezzeddine， D.（1996）。Proc。国家的。学会科学。美国93,589-595)。我们使用了一个再聚合培养系统来测试这个模型。将胚胎大鼠视网膜的祖细胞与过量的出生后视网膜细胞一起培养，然后分析它们的细胞命运选择。我们发现，出生后的环境至少有两个信号影响胚胎细胞的命运选择；一个信号抑制无毛细胞的产生，另一个信号影响锥细胞的产生。未观察到出生后产生的细胞类型增加。无毛细胞命运抑制剂的来源似乎是先前产生的无毛细胞，提示无毛细胞数量受反馈抑制控制。当祖细胞进入细胞周期的M期时，它失去了抑制无毛细胞产生的能力。我们认为，有丝分裂后细胞影响祖细胞的命运决定，但他们这样做的方式受到祖细胞的内在偏见的限制。
The seven major classes of cells of the vertebrate neural retina are generated from a pool of multipotent progenitor cells. Recent studies suggest a model of retinal development in which both the progenitor cells and the environment change over time (Cepko, C. L., Austin, C. P., Yang, X., Alexiades, M. and Ezzeddine, D. (1996). Proc. Natl. Acad. Sci. USA 93, 589-595). We have utilized a reaggregate culture system to test this model. A labeled population of progenitors from the embryonic rat retina were cultured with an excess of postnatal retinal cells and then assayed for their cell fate choices. We found that the postnatal environment had at least two signals that affected the embryonic cells' choice of fate; one signal inhibited the production of amacrine cells and a second affected the production of cone cells. No increase in cell types generated postnatally was observed. The source of the inhibitor of the amacrine cell fate appeared to be previously generated amacrine cells, suggesting that amacrine cell number is controlled by feedback inhibition. The progenitor cell lost its ability to be inhibited for production of an amacrine cell as it entered M phase of the cell cycle. We suggest that postmitotic cells influence progenitor cell fate decisions, but that they do so in a manner restricted by the intrinsic biases of progenitor cells.