Identification of Novel Drosophila Meiotic Genes Recovered in a P-Element Screen

Jeff Sekelsky(University of California, Davis), Kim S. McKim(Rutgers, The State University of New Jersey), Lisa G. Messina(University of California, Davis), Rachael L. French(University of North Carolina at Chapel Hill), Wendy D Hurley(University of California, Davis), Tamar Arbel(University of California, Davis), Gregory M. Chin(University of California, Davis), Benjamin Deneen(University of California, Los Angeles), Shelley J Force(University of California, Davis), Kumar L Hari(Salk Institute for Biological Studies), Janet K. Jang(Rutgers, The State University of New Jersey), Anne Laurençon(University of California, Davis), Laurence D Madden(Dartmouth College), H Matthies(University of California, Davis), Dawn B. Milliken(University of California, Davis), Scott L. Page(University of California, Davis), Amy D Ring(University of California, Davis), Sarah M. Wayson(University of California, Davis), Carin C Zimmerman(University of California, San Francisco), R. Scott Hawley(University of California, Davis)
Genetics
June 1, 1999
Cited by 90Open Access
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Abstract

The segregation of homologous chromosomes from one another is the essence of meiosis. In many organisms, accurate segregation is ensured by the formation of chiasmata resulting from crossing over. Drosophila melanogaster females use this type of recombination-based system, but they also have mechanisms for segregating achiasmate chromosomes with high fidelity. We describe a P-element mutagenesis and screen in a sensitized genetic background to detect mutations that impair meiotic chromosome pairing, recombination, or segregation. Our screen identified two new recombination-deficient mutations: mei-P22, which fully eliminates meiotic recombination, and mei-P26, which decreases meiotic exchange by 70% in a polar fashion. We also recovered an unusual allele of the ncd gene, whose wild-type product is required for proper structure and function of the meiotic spindle. However, the screen yielded primarily mutants specifically defective in the segregation of achiasmate chromosomes. Although most of these are alleles of previously undescribed genes, five were in the known genes alphaTubulin67C, CycE, push, and Trl. The five mutations in known genes produce novel phenotypes for those genes.


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