Processing of meiotic DNA recombination intermediates in Arabidopsis thaliana

• Applicant: Professor Dr. Holger Puchta
• Subject Area: Cell Biology
• Term: from 2009 to 2015
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 112721623

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.

• DFG Programme: Priority Programmes
• Subproject of: SPP 1384: Mechanisms of Genome Haploidisation