Lydall D, Nikolsky Y, Bishop D K, Weinert T
Department of Molecular and Cellular Biology, University of Arizona, Tucson 85721, USA.
Nature. 1996 Oct 31;383(6603):840-3. doi: 10.1038/383840a0.
In budding yeast, meiotic recombination occurs at about 200 sites per cell and involves DNA double-strand break (DSB) intermediates. Here we provide evidence that a checkpoint control requiring the mitotic DNA-damage checkpoint genes RAD17, RAD24 and MEC1 ensures that meiotic recombination is complete before the first meiotic division (MI). First, RAD17, RAD24 and MEC1 are required for the meiotic arrest caused by blocking the repair of DSBs with a mutation in the recA homologue DMC1. Second, mec1 and rad24 single mutants (DMC1+) appear to undergo MI before all recombination events are complete. Curiously, the mitosis-specific checkpoint gene RAD9 is not required for meiotic arrest of dmc1 mutants. This shows that although mitotic and meiotic control mechanisms are related, they differ significantly. Rad17 and Rad24 proteins may contribute directly to formation of an arrest signal by association with single-strand DNA in mitosis and meiosis.
在出芽酵母中，减数分裂重组大约在每个细胞的200个位点发生，并涉及DNA双链断裂（DSB）中间体。我们在此提供证据表明，一种需要有丝分裂DNA损伤检查点基因RAD17、RAD24和MEC1的检查点控制机制，可确保减数分裂重组在第一次减数分裂（MI）之前完成。首先，RAD17、RAD24和MEC1是通过recA同源物DMC1中的突变来阻断DSB修复所导致的减数分裂停滞所必需的。其次，mec1和rad24单突变体（DMC1+）似乎在所有重组事件完成之前就经历了MI。奇怪的是，有丝分裂特异性检查点基因RAD9对于dmc1突变体的减数分裂停滞并非必需。这表明，尽管有丝分裂和减数分裂控制机制相关，但它们存在显著差异。Rad17和Rad24蛋白可能通过在有丝分裂和减数分裂中与单链DNA结合，直接促进停滞信号的形成。
