ENHANCEMENT OF THE NCD(D) MICROTUBULE MOTOR MUTANT BY MUTANTS OF ALPHA-TUB67C

Ncd is a kinesin-related microtubule motor protein required for chromo some segregation in Drosophila oocytes and early embryos. In tests for interactions with other proteins, we find that mutants of alpha Tub67 C, which affect an oocyte- and early embryo-specific alpha-tubulin, en hance meiotic nondisjunction and zygotic loss of ncd(D), a partial los s-of-function mutant of ncd. The enhancement is dominant and allele-sp ecific with respect to alpha Tub67C, and depends on the recessive effe cts of ncd(D). Cytologically, embryos of alpha Tub67C/+ show delayed m eiotic divisions and defective female pronucleus formation, while meio tic spindle assembly is abnormal in embryos of ncd(D)/ncd(D). Doubly m utant alpha Tub67C ncd(D)/ncd(D) embryos are rescued for female pronuc leus formation, but show delayed meiotic progression and defective pro nuclear conjugation or fusion. Delayed completion of meiosis, together with failure of pronuclear fusion, prevents normal interactions of ma ternal with paternal chromosomes, enhancing the ncd(D) mutant phenotyp e. The genetics and cytology of doubly mutant embryos and the molecula r defect of Ncd(D) provide evidence for interaction of Ncd with alpha Tub67C in vivo. These results imply that a specific alpha-tubulin isof orm is required for normal cellular function of a kinesin motor protei n.