Control of Meiotic Homolog Segregation in Arabidopsis

拟南芥减数分裂同源分离的控制

• 批准号: 6368188
• 负责人: Hong Ma
• 金额: $ 25.43万
• 依托单位: PENNSYLVANIA STATE UNIVERSITY, THE
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-07-01 至 2005-06-30
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/6368188
• 关键词: Arabidopsis; chromosome movement; cyclin dependent kinase; cyclins; cytogenetics; gene expression; genetic regulation; meiosis; plant genetics; protein localization

DESCRIPTION (provided by the applicant): Meiotic homolog pairing and attachment are essential for normal chromosome segregation during meiosis I. It is thought that both meiotic recombination and sister chromatid cohesion are required for homolog attachment at late prophase I and metaphase I. Sister chromatid cohesion is removed from the chromosomal arms at the metaphase I/anaphase I transition, allowing homologs to separate. Arabidopsis is an excellent system to investigate the molecular control of meiosis because its available molecular genetic tools and the feasibility of good cytological studies. An Arabidopsis mutant, sds, was isolated and found to be defective in maintaining meiotic homolog attachment at prophase I. The SDS gene encodes a novel cyclin-like protein, suggesting that a cyclin-CDK complex is required for homolog attachment. In addition, it was shown that another Arabidopsis gene, ASK1, is required for release of homolog for separation at anaphase I, and that the ask1 mutant meiotic cells show persistent localization of the putative Arabidopsis meiotic cohesion SYN1 on chromosomes at late metaphase I and anaphase I. Preliminary evidence suggests that SDS may genetically interact with ASK1, supporting the hypothesis that SDS may also regulate the removal of cohesions from the chromosome. It is also possible that SDS may regulate meiotic recombination. These Arabidopsis mutant and genes will be used to gain new insights about the control of meiotic homolog attachment, using genetic, cytological and molecular approaches. Both cytological and genetic experiments will be carried out to test these hypotheses about SDS function. In addition, genetic interaction between SDS and SYN1and ASK1 will be investigated. Because SDS is a putative novel cyclin, additional experiments will be performed to test for interactions between SDS and CDKs, to probe for possible functions of CDKs in meiosis, and to identify and characterize genes what encode proteins that interact with SDS. Furthermore, molecular and cell biological experiments will be done to characterize the expression pattern and protein localization of SDS, and to isolate a putative SDS-like gene.

描述（由申请方提供）：减数分裂同源物配对和连接 是减数分裂I期间正常染色体分离所必需的。据认为 减数分裂重组和姐妹染色单体凝聚都是 在后期前期I和中期I有同源物附着。姐妹染色单体 在中期I/后期I，染色体臂上的凝聚力被去除 过渡，允许同系物分离。拟南芥是一个优秀的系统 研究减数分裂的分子控制，因为其可用的分子 遗传工具和良好的细胞学研究的可行性。拟南芥 分离到一个突变体SDS，发现它在维持减数分裂方面有缺陷 前期I的同源物附着。SDS基因编码一种新的细胞周期蛋白样蛋白 蛋白，这表明细胞周期蛋白-CDK复合物是同源物所必需的。 附件.此外，研究表明，另一个拟南芥基因ASK 1， 在后期I分离释放同系物所需的，并且ask 1 突变的减数分裂细胞表现出持续定位的假定拟南芥 减数分裂凝聚力SYN 1在晚中期I和后期I的染色体上。 初步证据表明SDS可能与ASK 1发生遗传相互作用， 支持SDS也可以调节内聚物去除的假设 从染色体上。SDS也可能参与减数分裂的调控 重组这些拟南芥突变体和基因将用于获得新的 关于控制减数分裂同源物附着的见解，使用遗传学， 细胞学和分子学方法。细胞学和遗传学实验 将进行测试这些假设的SDS功能。此外，本发明还提供了一种方法， 研究了SDS与SYN 1和ASK 1的遗传互作。因为 SDS是一种推定的新型细胞周期蛋白，将进行额外的实验， 测试SDS和CDK之间的相互作用，以探测 CDK在减数分裂中的作用，并鉴定和表征编码蛋白质的基因 与SDS相互作用。此外，分子和细胞生物学实验 将进行表征的表达模式和蛋白定位的 SDS，并分离一个推定的SDS样基因。