Processing of meiotic DNA recombination intermediates in Arabidopsis thaliana

拟南芥减数分裂 DNA 重组中间体的加工

• 批准号: 112721623
• 负责人: Professor Dr. Holger Puchta
• 金额: --
• 依托单位: Botanisches Institut
• 依托单位国家: 德国
• 项目类别: Priority Programmes
• 财政年份: 2009
• 资助国家: 德国
• 起止时间: 2008-12-31 至 2014-12-31
• 项目状态: 已结题
• 来源: https://gepris.dfg.de/gepris/projekt/112721623?language=en
• 关键词: Processing; meiotic; DNA; recombination; intermediates

During the first funding period, we analyzed the members of the RTR complex AtTOP3α and AtRMI1 in more detail, addressing the functional role of individual domains of the proteins in somatic and meiotic recombination as well as the genetic interaction with known meiotic recombination genes. Additionally we characterized the function of a homolog of a more recently discovered member of the RTR complex, AtRMI2, in genome stability and meiosis. In relation to our work on hyperrecombination suppression through the RTR complex, we started to analyze potential homologs of genetic or physical interaction partners of these genes. Here, we were able to identify plant homologs of the Fanconi anemia protein FANCM and of the animal antirecombinase RTEL1. In preliminary work, we could show that AtFANCM is involved in the suppression of somatic HR at stalled replication forks in a pathway parallel to that of RECQ4A. We discovered a surprising function of AtFANCM in meiotic recombination, where its mutation can suppress the sterile phenotype of Atmsh4 mutants. This points to a role of AtFANCM in the regulation of pathway choice between noncrossover and crossover out-comes in meiotic recombination that we would like to define further using a number of genetic and cytological methods. Arabidopsis possesses two unrelated antirecombinases AtSRS2 and AtRTEL1 that seem to act redundantly. Since rtel1 mutant plants show a fertility defect, we would like to investi-gate possible functions of this helicase in meiosis as well.

在第一个资助期间，我们更详细地分析了RTR复合物AtTOP 3 α和AtRMI 1的成员，解决了蛋白质的单个结构域在体细胞和减数分裂重组中的功能作用以及与已知减数分裂重组基因的遗传相互作用。此外，我们的特点是最近发现的成员的RTR复合物，AtRMI 2，在基因组稳定性和减数分裂的同源物的功能。关于我们通过RTR复合物抑制超重组的工作，我们开始分析这些基因的遗传或物理相互作用伴侣的潜在同源物。在这里，我们能够确定植物同源的范可尼贫血蛋白FANCM和动物抗重组酶RTEL1。在初步工作中，我们可以表明，AtFANCM参与抑制体细胞HR在停滞的复制叉在一个平行的途径RECQ4A。我们发现了AtFANCM在减数分裂重组中的一个令人惊讶的功能，其中它的突变可以抑制Atmsh4突变体的不育表型。这表明AtFANCM在减数分裂重组中非交换和交换结果之间的途径选择的调节中起作用，我们希望使用一些遗传学和细胞学方法进一步定义。拟南芥有两个不相关的反重组酶AtSRS2和AtRTEL1，似乎是冗余的。由于rtel 1突变体植物表现出育性缺陷，我们也想研究这种解旋酶在减数分裂中的可能功能。