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在果蝇中, vestigial 和 scalloped 之间的特定相互作用是促进翅组织增殖所必需的。

Specific interactions between vestigial and scalloped are required to promote wing tissue proliferation in Drosophila melanogaster.

作者信息

Paumard-Rigal S, Zider A, Vaudin P, Silber J

机构信息

Institut Jacques Monod, L.G.Q.M., 2, Place Jussieu, Tour 43, F-75251 Paris cedex 05, France.

出版信息

Dev Genes Evol. 1998 Oct;208(8):440-6. doi: 10.1007/s004270050201.

Abstract

The two genes vestigial (vg) and scalloped (sd) are required for wing development in Drosophila melanogaster. They present similar patterns of expression in second and third instar wing discs and similar wing mutant phenotypes. vg encodes a nuclear protein without any recognized nucleic acid-binding motif. Sd is a transcription factor homologous to the human TEF-1 factor whose promoter activity depends on cell-specific cofactors. We postulate that Vg could be a cofactor of Sd in the wing morphogenetic process and that, together, they could constitute a functional transcription complex. We investigated genetic interactions between the two genes. We show here that vg and sd co-operate in vivo in a manner dependent on the structure of the Vg protein. We ectopically expressed vg in the patch (ptc) domains. We show evidence that wing-like outgrowths induced by ectopic expression of vg are severely reduced in vg or sd mutant backgrounds. Accordingly, we demonstrate that ptc-GAL4-driven expression of vg induces both expressions of the endogenous vg and sd genes and that the two Vg and Sd proteins have to be produced together to promote wing proliferation. Furthermore, we show an interaction between the two proteins by double hybrid experiments in yeast. Our results therefore support the hypothesis that Sd and Vg directly interact in vivo to form a complex regulating the proliferation of wing tissue.

摘要

残翅(vg)和扇形翅(sd)这两个基因是黑腹果蝇翅膀发育所必需的。它们在二龄和三龄翅芽中呈现相似的表达模式,并且具有相似的翅膀突变表型。vg编码一种没有任何公认核酸结合基序的核蛋白。Sd是一种与人类TEF-1因子同源的转录因子,其启动子活性取决于细胞特异性辅因子。我们推测Vg可能是翅膀形态发生过程中Sd的辅因子,并且它们共同构成一个功能性转录复合体。我们研究了这两个基因之间的遗传相互作用。我们在此表明,vg和sd在体内以依赖于Vg蛋白结构的方式协同作用。我们在patched(ptc)结构域中异位表达vg。我们有证据表明,在vg或sd突变背景下,由vg异位表达诱导的翅膀样赘生物会严重减少。因此,我们证明ptc-GAL4驱动的vg表达会诱导内源性vg和sd基因的表达,并且两种Vg和Sd蛋白必须共同产生才能促进翅膀增殖。此外,我们通过酵母双杂交实验展示了这两种蛋白之间的相互作用。因此,我们的结果支持这样的假设:Sd和Vg在体内直接相互作用形成一个调节翅膀组织增殖的复合体。

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