Mutations in aurora prevent centrosome separation leading to the formation of monopolar spindles
Abstract
We show that female sterile mutations of aurora (aur) are allelic to mutations in the lethal complementation group ck¹⁰. This lies in a cytogenetic interval, 87A7-A9, that contains eight transcription units. A 250 by region upstream of both aur and a divergent transcription unit corresponds to the site of a specific chromatin structure (scs′) previously proposed to be a barrier to insulate enhancers of the major hsp70 gene at 87A7. Syncytial embryos derived from aur mothers display closely paired centrosomes at inappropriate mitotic stages and develop interconnected spindles in which the poles are shared. Amorphic alleles result in pupal lethality and in mitotic arrest in which condensed chromosomes are arranged on circular monopolar spindles. The size of the single centrosomal body in these circular figures suggests that loss of function of the serine-threonine protein kinase encoded by aur leads to a failure of the centrosomes to separate and form a bipolar spindle.
Additional Information
© 1995 by Cell Press. Under an Elsevier user license. Received 13 July 1994, Revised 5 February 1995. Correspondence should be addressed to D. M. G. This study was initiated during a visit by D. M. G. to Tübingen, Federal Republic of Germany, as a short-term European Molecular Biology Organization fellow in 1985. We wish to thank Christiane Nüsslein-Volhard for providing the aur alleles and for her encouragement in the early stages of this project. We wish to thank Janos Gausz (Szeged) for his gift of ck¹⁰ alleles and Andor Udvardy (Szeged) for his gift of cloned DNAs extending distally from 87A7. Cayetano Gonzalez provided assistance with the cytology of the 86•87 region and gave helpful advice throughout this project. Luke Alphey and Fiona Cullen kindly helped with DNA sequencing, and Will Whitfield helped with the real-time observations of mitosis following the injection of tagged histones into syncytial embryos. Part of this work, carried out in the Department of Biochemistry at Imperial College, was submitted by M. H. L. for his Ph.D. degree at the University of London in 1990. The body of the work has been supported by the Cancer Research Campaign, and we are also grateful to the Medical Research Council for a training fellowship to H. P. and for a research studentship to D. A. M.Additional details
- Eprint ID
- 104797
- DOI
- 10.1016/0092-8674(95)90374-7
- Resolver ID
- CaltechAUTHORS:20200806-163116598
- European Molecular Biology Organization (EMBO)
- Cancer Research Campaign
- Medical Research Council (UK)
- Created
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2020-08-10Created from EPrint's datestamp field
- Updated
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2021-11-16Created from EPrint's last_modified field