THE DROSOPHILA ROUGHENED MUTATION - ACTIVATION OF A RAP HOMOLOG DISRUPTS EYE DEVELOPMENT AND INTERFERES WITH CELL DETERMINATION
THE DROSOPHILA ROUGHENED MUTATION - ACTIVATION OF A RAP HOMOLOG DISRUPTS EYE DEVELOPMENT AND INTERFERES WITH CELL DETERMINATION
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DOI：
10.1016/0092-8674(91)90066-8
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发表时间：
1991-11-15
期刊：
影响因子：
64.5
通讯作者：
RUBIN, GM
中科院分区：
文献类型：
--
作者：
HARIHARAN, IK;CARTHEW, RW;RUBIN, GM
糙化是黑腹龙的显性突变，它会破坏眼睛的发育。成人眼的大多数小眼缺少一个感光细胞，最常见的是R7细胞。粗糙突变破坏了感光细胞决定的早期阶段。粗化是一种显性的功能获得突变，它是由果蝇Rap1蛋白的一个氨基酸变化（Phe157到Leu）引起的。功能丧失Rap1突变是致命的。果蝇Rap1蛋白与人类rap1A/K-rev1蛋白88%相同，rap1A/K-rev1蛋白被认为是ras作用的拮抗剂。
Roughened is a dominant mutation of D. melanogaster that disrupts eye development. The majority of the ommatidia in the adult eye lack a single photoreceptor cell, which is most commonly the R7 cell. The Roughened mutation disrupts the early stages of photoreceptor cell determination. Roughened is a dominant gain-of-function mutation that results from a single amino acid change (Phe157 to Leu) in the Drosophila Rap1 protein. Loss of function Rap1 mutations are lethal. Drosophila Rap1 protein is 88% identical to human rap1A/K-rev1 protein, a putative antagonist of ras action.