Journal of Cell Science, Vol 110, Issue 8 945-954, Copyright © 1997 by Company of Biologists

JOURNAL ARTICLES

Mutation of a gene for a Drosophila kinesin-like protein, Klp38B, leads to failure of cytokinesis

H Ohkura, T Torok, G Tick, J Hoheisel, I Kiss and DM Glover
CRC Cell Cycle Genetics Group, Department of Anatomy and Physiology, The University of Dundee, UK.

Mutations in a gene (Klp38B) encoding a novel kinesin-like protein in Drosophila melanogaster lead to the formation of polyploid cells in the larval central nervous system and in the follicle cells of adult egg chambers. Some homozygous mutants survive to adulthood and also exhibit morphological defects indicative of abnormal cell cycle progression, including rough eyes, missing bristles, and abnormal abdominal cuticles. In larval brains, there is no accumulation of mitotic cells and the frequency of anaphase figures is comparable to wild type, suggesting that nuclear division is not affected. Such brains contain polyploid cells with metaphase and anaphase chromosomes associated with bipolar spindles. Such spindles have a number of unseparated centrosomes at their poles reflecting the degree of polyploidy of the cell. Follicle cells frequently contain two nuclei of roughly equal size. Taken together, we conclude that these Klp38B mutations lead to a failure of cytokinesis resulting in polyploidy, and discuss whether or not this is a direct effect of the mutation.
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