Yadav Vikash Kumar, Claeys Bouuaert Corentin
Louvain Institute of Biomolecular Science and Technology, Université catholique de Louvain, Louvain-La-Neuve, Belgium.
Front Cell Dev Biol. 2021 Mar 2;9:642737. doi: 10.3389/fcell.2021.642737. eCollection 2021.
Developmentally programmed formation of DNA double-strand breaks (DSBs) by Spo11 initiates a recombination mechanism that promotes synapsis and the subsequent segregation of homologous chromosomes during meiosis. Although DSBs are induced to high levels in meiosis, their formation and repair are tightly regulated to minimize potentially dangerous consequences for genomic integrity. In , nine proteins participate with Spo11 in DSB formation, but their molecular functions have been challenging to define. Here, we describe our current view of the mechanism of meiotic DSB formation based on recent advances in the characterization of the structure and function of DSB proteins and discuss regulatory pathways in the light of recent models.
由Spo11介导的DNA双链断裂（DSB）的发育程序性形成启动了一种重组机制，该机制在减数分裂过程中促进同源染色体的联会及随后的分离。尽管在减数分裂中DSB被诱导到高水平，但其形成和修复受到严格调控，以将对基因组完整性的潜在危险后果降至最低。在[具体内容缺失]中，九种蛋白质与Spo11一起参与DSB的形成，但其分子功能一直难以确定。在此，我们基于DSB蛋白结构和功能表征的最新进展描述了我们目前对减数分裂DSB形成机制的看法，并根据最新模型讨论调控途径。
