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The Journal of Cell Biology, Vol 123, 665-679, Copyright © 1993 by The Rockefeller University Press
ARTICLES |
MM Heck, A Pereira, P Pesavento, Y Yannoni, AC Spradling and LS Goldstein
Johns Hopkins University, School of Medicine, Department of Cell Biology and Anatomy, Baltimore, Maryland 21205.
We report here that disruption of a recently discovered kinesin-like protein in Drosophila melanogaster, KLP61F, results in a mitotic mutation lethal to the organism. We show that in the absence of KLP61F function, spindle poles fail to separate, resulting in the formation of monopolar mitotic spindles. The resulting phenotype of metaphase arrest with polyploid cells is reminiscent of that seen in the fungal bimC and cut7 mutations, where it has also been shown that spindle pole bodies are not segregated. KLP61F is specifically expressed in proliferating tissues during embryonic and larval development, consistent with a primary role in cell division. The structural and functional homology of the KLP61F, bimC, cut7, and Eg5 kinesin-like proteins demonstrates the existence of a conserved family of kinesin-like molecules important for spindle pole separation and mitotic spindle dynamics.
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