Second-site noncomplementation identifies genomic regions required for Drosophila nonmuscle myosin function during morphogenesis.
Second-site noncomplementation identifies genomic regions required for Drosophila nonmuscle myosin function during morphogenesis.
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第二位点非互补识别了果蝇形态发生过程中非肌肉肌球蛋白功能所需的基因组区域。
DOI：
10.1093/genetics/148.4.1845
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发表时间：
1998
期刊：
影响因子：
3.3
通讯作者：
Kiehart,DP
中科院分区：
文献类型：
--
作者：
Halsell,SR;Kiehart,DP
果蝇是分析非肌球蛋白- ii（以下简称肌球蛋白）在发育过程中作用的理想后生动物模型系统。在果蝇中，在卵发生、胚胎发生、幼虫发育和蛹蜕变过程中，由细胞迁移和/或细胞形状变化驱动的细胞分裂和形态发生需要肌球蛋白的功能。调节肌凝蛋白功能的机制和肌凝蛋白结合的超分子结构尚未被系统地表征。这里描述的遗传筛选鉴定揭示促进肌凝蛋白功能的位点的基因组区域。非肌球蛋白重链是由一个单一位点编码的。在畸形表型的二位点非互补分析中，对占约70%的常染色质基因组的连续染色体缺陷进行了筛选，以确定其与zipper的两个隐性致死等位基因的遗传相互作用。成人腿部的畸形反映了在腿部形态发生过程中由肌球蛋白基础收缩驱动的细胞形状变化的畸变。在测试的158个缺陷中，47个表现为拉链的第二位点非互补。其中2个是强相互作用体，17个是中等相互作用体，28个是弱相互作用体。更精细的遗传定位显示，细胞质原肌球蛋白和IV型胶原蛋白的突变在腿部形态发生过程中充当了zipper的第二位点非互补体，而zipper的功能需要一个以前未被表征的位点E3.10/J3.8来进行腿部形态发生和生存。
Drosophila is an ideal metazoan model system for analyzing the role of nonmuscle myosin-II (henceforth, myosin) during development. In Drosophila, myosin function is required for cytokinesis and morphogenesis driven by cell migration and/or cell shape changes during oogenesis, embryogenesis, larval development and pupal metamorphosis. The mechanisms that regulate myosin function and the supramolecular structures into which myosin incorporates have not been systematically characterized. The genetic screens described here identify genomic regions that uncover loci that facilitate myosin function. The nonmuscle myosin heavy chain is encoded by a single locus, zipper. Contiguous chromosomal deficiencies that represent approximately 70% of the euchromatic genome were screened for genetic interactions with two recessive lethal alleles of zipper in a second-site noncomplementation assay for the malformed phenotype. Malformation in the adult leg reflects aberrations in cell shape changes driven by myosin-based contraction during leg morphogenesis. Of the 158 deficiencies tested, 47 behaved as second-site noncomplementors of zipper. Two of the deficiencies are strong interactors, 17 are intermediate and 28 are weak. Finer genetic mapping reveals that mutations in cytoplasmic tropomyosin and viking (collagen IV) behave as second-site noncomplementors of zipper during leg morphogenesis and that zipper function requires a previously uncharacterized locus, E3.10/J3.8, for leg morphogenesis and viability.