Female sterile mutations on the second chromosome of Drosophila melanogaster. I. Maternal effect mutations.
Female sterile mutations on the second chromosome of Drosophila melanogaster. I. Maternal effect mutations.
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DOI：
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发表时间：
1989
期刊：
影响因子：
3.3
通讯作者：
Trudi Schüpbach;Eric Wieschaus
中科院分区：
文献类型：
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作者：
Trudi Schüpbach;Eric Wieschaus
在黑腹果蝇第二条染色体上隐性雌性不育突变的诱变筛选中，分离出529条染色体，这些染色体允许纯合雌性存活，但导致它们不育。在这些品系中的136个中，突变的雌性产生形态上正常的卵子，这些卵子不能支持正常的胚胎发育。这些“母亲效应”突变属于67个互补组，它们定义了23个多重命中位点和44个单命中位点。在14个互补组的卵子中，发育在合胞胚盘形成之前被阻断。12个互补群的卵细胞化前发育异常，17个互补群引起细胞化异常，12个互补群引起原肠胚形成早期细胞形态的变化，12个互补群似乎影响后期胚胎发育。
In mutagenesis screens for recessive female sterile mutations on the second chromosome of Drosophila melanogaster 529 chromosomes were isolated which allow the homozygous females to survive, but cause them to be sterile. In 136 of these lines, mutant females produce morphologically normal eggs which cannot support normal embryonic development. These "maternal-effect" mutations fall into 67 complementation groups which define 23 multiply hit and 44 singly hit loci. In eggs from 14 complementation groups development is blocked before the formation of a syncytial blastoderm. In eggs from 12 complementation groups development is abnormal before cellularization, 17 complementation groups cause abnormal cellularization, 12 complementation groups cause changes in cellular morphology in early gastrulation stages, and 12 complementation groups seem to affect later embryonic development.