Vignard Julien, Siwiec Tanja, Chelysheva Liudmila, Vrielynck Nathalie, Gonord Florine, Armstrong Susan J, Schlögelhofer Peter, Mercier Raphael
Station de Génétique et d'Amélioration des Plantes, INRA, Versailles, France.
PLoS Genet. 2007 Oct;3(10):1894-906. doi: 10.1371/journal.pgen.0030176. Epub 2007 Aug 30.
During meiosis, homologous chromosomes recognize each other, align, and exchange genetic information. This process requires the action of RecA-related proteins Rad51 and Dmc1 to catalyze DNA strand exchanges. The Mnd1-Hop2 complex has been shown to assist in Dmc1-dependent processes. Furthermore, higher eukaryotes possess additional RecA-related proteins, like XRCC3, which are involved in meiotic recombination. However, little is known about the functional interplay between these proteins during meiosis. We investigated the functional relationship between AtMND1, AtDMC1, AtRAD51, and AtXRCC3 during meiosis in Arabidopsis thaliana. We demonstrate the localization of AtMND1 to meiotic chromosomes, even in the absence of recombination, and show that AtMND1 loading depends exclusively on AHP2, the Arabidopsis Hop2 homolog. We provide evidence of genetic interaction between AtMND1, AtDMC1, AtRAD51, and AtXRCC3. In vitro assays suggest that this functional link is due to direct interaction of the AtMND1-AHP2 complex with AtRAD51 and AtDMC1. We show that AtDMC1 foci accumulate in the Atmnd1 mutant, but are reduced in number in Atrad51 and Atxrcc3 mutants. This study provides the first insights into the functional differences of AtRAD51 and AtXRCC3 during meiosis, demonstrating that AtXRCC3 is dispensable for AtDMC1 focus formation in an Atmnd1 mutant background, whereas AtRAD51 is not. These results clarify the functional interactions between key players in the strand exchange processes during meiotic recombination. Furthermore, they highlight a direct interaction between MND1 and RAD51 and show a functional divergence between RAD51 and XRCC3.
在减数分裂过程中,同源染色体相互识别、对齐并交换遗传信息。这一过程需要RecA相关蛋白Rad51和Dmc1发挥作用来催化DNA链交换。已证明Mnd1-Hop2复合体有助于依赖Dmc1的过程。此外,高等真核生物还拥有其他RecA相关蛋白,如XRCC3,它们参与减数分裂重组。然而,对于这些蛋白在减数分裂过程中的功能相互作用知之甚少。我们研究了拟南芥减数分裂过程中AtMND1、AtDMC1、AtRAD51和AtXRCC3之间的功能关系。我们证明了即使在没有重组的情况下,AtMND1也定位于减数分裂染色体上,并表明AtMND1的加载完全依赖于拟南芥Hop2同源物AHP2。我们提供了AtMND1、AtDMC1、AtRAD51和AtXRCC3之间遗传相互作用的证据。体外试验表明,这种功能联系是由于AtMND1-AHP2复合体与AtRAD51和AtDMC1的直接相互作用。我们发现AtDMC1焦点在Atmnd1突变体中积累,但在Atrad51和Atxrcc3突变体中的数量减少。这项研究首次揭示了AtRAD51和AtXRCC3在减数分裂过程中的功能差异,表明在Atmnd1突变体背景下,AtXRCC3对于AtDMC1焦点形成是可有可无的,而AtRAD51则不是。这些结果阐明了减数分裂重组过程中链交换过程关键参与者之间的功能相互作用。此外,它们突出了MND1和RAD51之间的直接相互作用,并显示了RAD51和XRCC3之间的功能差异。