Komma D J, Endow S A
Department of Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
J Cell Sci. 1997 Jan;110 ( Pt 2):229-37. doi: 10.1242/jcs.110.2.229.
Ncd is a kinesin-related microtubule motor protein required for chromosome segregation in Drosophila oocytes and early embryos. In tests for interactions with other proteins, we find that mutants of alpha Tub67C, which affect an oocyte- and early embryo-specific alpha-tubulin, enhance meiotic nondisjunction and zygotic loss of ncdD, a partial loss-of-function mutant of ncd. The enhancement is dominant and allele-specific with respect to alpha Tub67C, and depends on the recessive effects of ncdD. Cytologically, embryos of alpha Tub67C/+ show delayed meiotic divisions and defective female pronucleus formation, while meiotic spindle assembly is abnormal in embryos of ncdD/ncdD. Doubly mutant alpha Tub67C ncdD/ncdD embryos are rescued for female pronucleus formation, but show delayed meiotic progression and defective pronuclear conjugation or fusion. Delayed completion of meiosis, together with failure of pronuclear fusion, prevents normal interactions of maternal with paternal chromosomes, enhancing the ncdD mutant phenotype. The genetics and cytology of doubly mutant embryos and the molecular defect of NcdD provide evidence for interaction of Ncd with alpha Tub67C in vivo. These results imply that a specific alpha-tubulin isoform is required for normal cellular function of a kinesin motor protein.
Ncd是一种与驱动蛋白相关的微管运动蛋白，在果蝇卵母细胞和早期胚胎的染色体分离过程中发挥作用。在与其他蛋白质相互作用的测试中，我们发现，影响卵母细胞和早期胚胎特异性α-微管蛋白的αTub67C突变体，会增强减数分裂不分离现象以及ncdD（一种ncd的部分功能丧失突变体）的合子损失。这种增强作用对于αTub67C而言是显性且等位基因特异性的，并且依赖于ncdD的隐性效应。从细胞学角度来看，αTub67C/+胚胎的减数分裂延迟，雌性原核形成存在缺陷，而ncdD/ncdD胚胎的减数分裂纺锤体组装异常。双突变αTub67C ncdD/ncdD胚胎的雌性原核形成得到挽救，但减数分裂进程延迟，原核结合或融合存在缺陷。减数分裂延迟完成，再加上原核融合失败，会阻止母本与父本染色体的正常相互作用，从而增强ncdD突变体表型。双突变胚胎的遗传学和细胞学以及NcdD的分子缺陷，为Ncd与αTub67C在体内的相互作用提供了证据。这些结果表明，一种特定的α-微管蛋白异构体是驱动蛋白运动蛋白正常细胞功能所必需的。
