Published May 19, 1997 | Published
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The Drosophila Gene abnormal spindle Encodes a Novel Microtubule-associated Protein That Associates with the Polar Regions of the Mitotic Spindle

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Abstract

abnormal spindle, a gene required for normal spindle structure and function in Drosophila melanogaster, lies immediately adjacent the gene tolloid at 96A/B. It encodes a 220-kD polypeptide with a predicted pI of 10.8. The recessive mutant allele asp1 directs the synthesis of a COOH terminally truncated or internally deleted peptide of ∼124 kD. Wild-type Asp protein copurifies with microtubules and is not released by salt concentrations known to dissociate most other microtubule-associated proteins. The bacterially expressed NH2-terminal 512-amino acid peptide, which has a number of potential phosphorylation sites for p34cdc2 and MAP kinases, strongly binds to microtubules. The central 579-amino acid segment of the molecule contains one short motif homologous to sequences in a number of actin bundling proteins and a second motif present at the calmodulin binding sites of several proteins. Immunofluorescence studies show that the wild-type Asp protein is localized to the polar regions of the spindle immediately surrounding the centrosome. These findings are discussed in relation to the known spindle abnormalities in asp mutants.

Additional Information

© 1997 The Rockefeller University Press. 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 5 October 1996 and in revised form 30 January 1997. We would like to thank Fiona Cullen for sequencing; Mar Carmena and Daryl Henderson for their comments on the manuscript; Alvaro Tavares for his suggestions and help; and Dr. M. O'Connor for supplying lines transformed with pMBO1366 and pMBO1367. This work was supported by research grants from Science and Engineering Research Council, Medical Research Council, Cancer Research Campaign, and the Human Capital and Mobility Programme of the European Union. Thomas Howard is grateful for a studentship from BBSRC and Maria do Carmo Avides for an European Molecular Biology Laboratory Long-Term Fellowship.

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