Takamune T Saito, Koki Yamamoto, Hirohito Minami, Taiki Tsujiue
{"title":"<i>Caenorhabditis elegans brc-1</i> mutation increases the number of COSA-1 foci in <i>him-8</i> and <i>zim-2</i> mutants.","authors":"Takamune T Saito, Koki Yamamoto, Hirohito Minami, Taiki Tsujiue","doi":"10.17912/micropub.biology.001077","DOIUrl":null,"url":null,"abstract":"<p><p>Crossover designation factors such as COSA-1 are concentrated at the specific DNA double-strand break (DSB) sites to promote crossover formation. <i>zim-1</i> mutants, which show defects in the homologous chromosome pairing of chromosomes II and III, increase the COSA-1 foci/normal bivalent state compared to the expected value. The excess designation was suppressed by an additional mutation in <i>brc-1</i> in <i>zim-1</i> mutants. We demonstrated that the number of COSA-1 foci in <i>him-8</i> and <i>zim-2</i> mutants, showing defects in the pairing of the X and V chromosomes, respectively, increased compared to the expected value, and <i>brc-1</i> mutation accelerated the number of COSA-1 foci in oogenesis.</p>","PeriodicalId":74192,"journal":{"name":"microPublication biology","volume":"2024 ","pages":""},"PeriodicalIF":0.0000,"publicationDate":"2024-07-25","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"https://www.ncbi.nlm.nih.gov/pmc/articles/PMC11310775/pdf/","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"microPublication biology","FirstCategoryId":"1085","ListUrlMain":"https://doi.org/10.17912/micropub.biology.001077","RegionNum":0,"RegionCategory":null,"ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"2024/1/1 0:00:00","PubModel":"eCollection","JCR":"","JCRName":"","Score":null,"Total":0}
引用次数: 0
Abstract
Crossover designation factors such as COSA-1 are concentrated at the specific DNA double-strand break (DSB) sites to promote crossover formation. zim-1 mutants, which show defects in the homologous chromosome pairing of chromosomes II and III, increase the COSA-1 foci/normal bivalent state compared to the expected value. The excess designation was suppressed by an additional mutation in brc-1 in zim-1 mutants. We demonstrated that the number of COSA-1 foci in him-8 and zim-2 mutants, showing defects in the pairing of the X and V chromosomes, respectively, increased compared to the expected value, and brc-1 mutation accelerated the number of COSA-1 foci in oogenesis.