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果蝇中变形功能修饰因子的筛选。

A screen for modifiers of Deformed function in Drosophila.

作者信息

Harding K W, Gellon G, McGinnis N, McGinnis W

机构信息

Department of Molecular Biophysics and Biochemistry, Yale University, New Haven Connecticut 06520-8114, USA.

出版信息

Genetics. 1995 Aug;140(4):1339-52. doi: 10.1093/genetics/140.4.1339.

DOI:10.1093/genetics/140.4.1339
PMID:7498774
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC1206698/
Abstract

Proteins produced by the homeotic genes of the Hox family assign different identifies to cells on the anterior/posterior axis. Relatively little is known about the signalling pathways that modulate their activities or the factors with which they interact to assign specific segmental identifies. To identify genes that might encode such functions, we performed a screen for second site mutations that reduce the viability of animals carrying hypomorphic mutant alleles of the Drosophila homeotic locus, Deformed. Genes mapping to six complementation groups on the third chromosome were isolated as modifiers of Deformed function. Products of two of these genes, sallimus and moira, have been previously proposed as homeotic activators since they suppress the dominant adult phenotype of Polycomb mutants. Mutations in hedgehog, which encodes secreted signalling proteins, were also isolated as Deformed loss-of-function enhancers. Hedgehog mutant alleles also suppress the Polycomb phenotype. Mutations were also isolated in a few genes that interact with Deformed but not with Polycomb, indicating that the screen identified genes that are not general homeotic activators. Two of these genes, cap 'n' collar and defaced, have defects in embryonic head development that are similar to defects seen in loss of function Deformed mutants.

摘要

由Hox家族的同源异型基因产生的蛋白质为前后轴上的细胞赋予不同的身份。对于调节其活性的信号通路或与它们相互作用以赋予特定节段身份的因子,我们了解得相对较少。为了鉴定可能编码此类功能的基因,我们对降低携带果蝇同源异型基因座Deformed的亚效突变等位基因的动物活力的第二位点突变进行了筛选。定位到第三条染色体上六个互补群的基因被分离出来作为Deformed功能的修饰因子。其中两个基因sallimus和moira的产物先前已被认为是同源异型激活因子,因为它们抑制了多梳突变体的显性成虫表型。编码分泌信号蛋白的刺猬基因(hedgehog)中的突变也被分离出来作为Deformed功能丧失的增强子。刺猬基因的突变等位基因也抑制多梳表型。在一些与Deformed相互作用但不与多梳相互作用的基因中也分离到了突变,这表明该筛选鉴定出的基因不是一般的同源异型激活因子。其中两个基因,cap 'n' collar和defaced,在胚胎头部发育中存在缺陷,这些缺陷与功能丧失的Deformed突变体中观察到的缺陷相似。

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