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Published October 1991 | Published
Journal Article Open

Chromosome tangling and breakage at anaphase result from mutations in lodestar, a Drosophila gene encoding a putative nucleoside triphosphate-binding protein

Abstract

We describe a Drosophila maternal-effect gene, lodestar, mutations in which cause chromatin bridges at anaphase. lodestar maps to cytological position 84D13-14, and we identified the lodestar gene in germ-line transformation experiments by the ability of a genomic fragment to restore fertility to females homozygous for lodestar mutations. lodestar encodes a potential nucleoside triphosphate binding protein, which is a novel member of the D-E-A-H box family of proteins. Antibodies raised against the lodestar gene product detect a protein that undergoes cell cycle-dependent changes in distribution in the embryo. The protein is cytoplasmic at interphase, and rapidly enters the nucleus early in prophase. It is restricted to the region enclosed by the spindle envelope during metaphase and anaphase; but by telophase, the lodestar protein is contained entirely within the reforming nucleus.

Additional Information

© 1991 Cold Spring Harbor Laboratory Press. The Authors acknowledge that six months after the full-issue publication date, the Article will be distributed under a Creative Commons CC-BY-NC License (Attribution-NonCommercial 4.0 International License, http://creativecommons.org/licenses/by-nc/4.0/). Received July 1, 1991; revised version accepted August 15, 1991. We are grateful to Christiane Nüsslein-Volhard for providing lodestar alleles, and to Mark Liebowitz and Jordan Raft for their initial phenotypic characterization of the mutants. Bruce Baker generously provided all of the cloned DNA from the region and several additional cDNA clones; he also communicated many unpublished results. We are grateful to Jordan Raff for the gift of the RNA used for Northern blotting and to Kevin O'Hare for providing the Northern blot of RNA from the dysgenic cross (Fig. 4C). The 0- to 4-hr embryo eDNA library was the kind gift of Nicholas Brown. The PESTFIND computer program was a gift of Martin Rechsteiner. We thank Cayetano Gonzalez, Brian Dalby, and Gabriela Maldonado-Codina for their comments on the manuscript. C.H.G. received a studentship from the Science and Engineering Research Council and postdoctoral support from the Cancer Research Campaign. This research was funded by the Cancer Research Campaign. The publication costs of this article were defrayed in part by payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 USC section 1734 solely to indicate this fact.

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