Genetic analysis of photoreceptor cell development in the zebrafish retina
Genetic analysis of photoreceptor cell development in the zebrafish retina
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DOI：
10.1016/s0925-4773(01)00571-8
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发表时间：
2002-01-01
影响因子：
2.6
通讯作者：
Malicki, J
中科院分区：
文献类型：
--
作者：
Doerre, G;Malicki, J
为了深入了解光感受器发育的遗传机制，我们分析了一系列以早期光感受器细胞丢失为特征的斑马鱼突变。突变缺陷损害了外节的形成，并伴有视觉色素的异常分布。视杆细胞和不同类型的视锥细胞表现出相似严重程度的缺陷，表明所有光感受器共有的遗传途径受到影响。为了研究这些表型是否涉及细胞与细胞相互作用缺陷，我们分析了基因嵌合动物，niezerka光感受器与野生型组织的相互作用提高了突变细胞的存活率并恢复了其细长的形态。相比之下，在布鲁达、椭圆、弗莱尔和椭圆形基因座中携带突变的细胞在野生型环境中保留其缺陷表型，表明细胞自主性。这些实验鉴定了光感受器突变体的不同表型类别，并表明斑马鱼光感受器缺陷涉及细胞自主和细胞非自主机制。 (C) 2002 Elsevier Science Ireland Ltd. 保留所有权利。
To gain insight into the genetic mechanisms of photoreceptor development, we analyzed a collection of zebrafish mutations characterized by early photoreceptor cell loss. The mutant defects impair outer segment formation and are accompanied by an abnormal distribution of visual pigments. Rods and different cone types display defects of similar severity suggesting that genetic pathways common to all photoreceptors are affected. To investigate whether these phenotypes involve cell-cell interaction defects, we analyzed genetically mosaic animals, Interaction of niezerka photoreceptors with wild-type tissues improves the survival of mutant cells and restores their elongated morphology. In contrast, cells carrying mutations in the loci brudas, elipsa, fleer, and oval retain their defective phenotypes in a wild-type environment indicating cell-autonomy. These experiments identify distinct phenotypic categories of photoreceptor mutants and indicate that zebrafish photoreceptor defects involve both cell-autonomous and cell-nonautonomous mechanisms. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.