rough deal: a gene required for proper mitotic segregation in Drosophila
- Creators
- Karess, Roger E.
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Glover, David M.
Abstract
We describe a genetic locus rough deal (rod) in Drosophila melanogaster, identified by mutations that interfere with the faithful transmission of chromosomes to daughter cells during mitosis. Five mutant alleles were isolated, each associated with a similar set of mitotic abnormalities in the dividing neuroblasts of homozygous mutant larvae: high frequencies of aneuploid cells and abnormal anaphase figures, in which chromatids may lag, form bridges, or completely fail to separate. Surviving homozygous adults are sterile, and show cuticular defects associated with cell death, i.e., roughened eyes, sparse abdominal bristles, and notched wing margins. The morphological process of spermatogenesis is largely unaffected and motile sperm are produced, but meiocyte aneuploidy is common. The nature of the observed abnormalities in mitotic cells suggests that the reduced fidelity of chromosome transmission to the daughter cells is due to a failure in a mechanism involved in assuring the proper release of sister chromatids.
Additional Information
© The Rockefeller University Press 1989. After the Initial Publication Period, RUP will grant to the public the non-exclusive right to copy, distribute, or display the Article under a Creative Commons Attribution-Noncommercial-Share Alike 4.0 International license, as described at https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode, or updates thereof. Received for publication 15 May 1989 and in revised form 14 August 1989. The authors gratefully acknowledge the excellent and diligent technical assistance of Alan Cheshire and Isabel Aguilera, as well as the stimulating mitotic discussions with M. Axton, A. Carpenter, P. D'Eustachio, C. Gonzalez, S. Hawley, H. Klein, and C. Sunkel. We thank T. Strecker, L. Goldstein, and A. Shearn for supplying fly stocks. This work was supported in part by a grant from the Medical Research Council of Great Britain. R. E. Karess was supported in the United States by grant GM37979 from the National Institutes of Health and a scholarship from the Pew Charitable Trust.Attached Files
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Additional details
- PMCID
- PMC2115894
- Eprint ID
- 105817
- Resolver ID
- CaltechAUTHORS:20201005-143650328
- Medical Research Council (UK)
- NIH
- GM37979
- Pew Charitable Trust
- Created
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2020-10-05Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field