Rogge R, Cagan R, Majumdar A, Dulaney T, Banerjee U
Department of Biology, University of California, Los Angeles 90024.
Proc Natl Acad Sci U S A. 1992 Jun 15;89(12):5271-5. doi: 10.1073/pnas.89.12.5271.
Mutations in a gene called sextra (sxt) have been isolated. Loss of one copy of sxt promotes R7 photoreceptor cell development in a genetically sensitized background, while loss of both copies results in precursors of non-neuronal cone cells transforming into R7 cells. The requirement for sxt function is cell-autonomous. The transformation of cone-cell precursors into R7 cells occurs independently of the sevenless signal. However, the R7 precursor becomes neuronal in an sxt/sxt mutant only in a wild-type sevenless background. The genetic analysis of sxt suggests that it plays an inhibitory role, preventing cone cells from becoming neuronal. Additionally, sxt functions in R7 precursors, but the sevenless signal is essential for specification of this fate, since loss of sextra alone is unable to impart a neural fate to this cell.
已分离出一种名为sextra(sxt)的基因突变体。在遗传敏感背景下,sxt基因单拷贝缺失会促进R7光感受器细胞发育,而两个拷贝均缺失则会导致非神经元视锥细胞前体转变为R7细胞。sxt功能的需求是细胞自主的。视锥细胞前体向R7细胞的转变独立于sevenless信号发生。然而,只有在野生型sevenless背景下,R7前体细胞在sxt/sxt突变体中才会变成神经元细胞。对sxt的遗传分析表明,它起抑制作用,阻止视锥细胞变成神经元细胞。此外,sxt在R7前体细胞中发挥作用,但sevenless信号对于这种命运的决定至关重要,因为仅sxt缺失无法赋予该细胞神经命运。