激酶 ATR 在拟南芥基因组尺度上控制减数分裂交叉分布

Longfei Zhu, Julia Dluzewska, Nadia Fernández-Jiménez, Rajeev Ranjan, Alexandre Pelé, Wojciech Dziegielewski, Maja Szymanska-Lejman, Karolina Hus, Julia Górna, Mónica Pradillo, Piotr A Ziolkowski
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引用次数: 0

摘要

减数分裂交叉,即减数分裂过程中染色体片段的相互交换,是遗传多样性的关键驱动因素。交叉是由程序性 DNA 双链断裂(DSB)的形成启动的。虽然ATAXIA-TELANGIECTASIA和RAD3-RELATED(ATR)激酶在DNA损伤信号转导中的作用众所周知,但它对交叉形成的影响仍未得到充分研究。在这里,我们利用染色体间隔重组测量和全基因组交叉图谱研究表明,拟南芥(Arabidopsis thaliana)中 ATR 失活会导致显著的交叉重新分布,染色体臂上的交叉频率增加,而中心粒周围的交叉频率降低。我们通过分析拟南芥中磷酸化的H2A.X病灶证明,这些交叉位置的整体变化并不是由DSB数量的改变引起的。利用种子分型技术,我们发现与野生型个体相比,atr 突变体中的热点使用情况主要保持不变。此外,atr 在两个独立途径引起的交叉数量上没有变化,这意味着它对交叉途径的选择没有影响。遗传交互作用分析表明,虽然atr的影响独立于MMS和UV SENSITIVE81(MUS81)、ZIPPER1(ZYP1)、FANCONI ANEMIA COMPLEMENTATION GROUP M(FANCM)和D2(FANCD2),但ATR和FANCD2的潜在机制可能相似。这项研究拓展了我们对 ATR 在减数分裂中作用的认识,发现了其在调节交叉分布方面的功能。
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The kinase ATR controls meiotic crossover distribution at the genome scale in Arabidopsis
Meiotic crossover, i.e., the reciprocal exchange of chromosome fragments during meiosis, is a key driver of genetic diversity. Crossover is initiated by the formation of programmed DNA double-strand breaks (DSBs). While the role of ATAXIA-TELANGIECTASIA AND RAD3-RELATED (ATR) kinase in DNA damage signaling is well-known, its impact on crossover formation remains understudied. Here, using measurements of recombination at chromosomal intervals and genome-wide crossover mapping, we showed that ATR inactivation in Arabidopsis (Arabidopsis thaliana) leads to dramatic crossover redistribution, with an increase in crossover frequency in chromosome arms and a decrease in pericentromeres. These global changes in crossover placement were not caused by alterations in DSB numbers, which we demonstrated by analyzing phosphorylated H2A.X foci in zygonema. Using the seed-typing technique, we found that hotspot usage remains mainly unchanged in atr mutants compared to wild-type individuals. Moreover, atr showed no change in the number of crossovers caused by two independent pathways, which implies no effect on crossover pathway choice. Analyses of genetic interaction indicate that while the effects of atr are independent of MMS AND UV SENSITIVE81 (MUS81), ZIPPER1 (ZYP1), FANCONI ANEMIA COMPLEMENTATION GROUP M (FANCM) and D2 (FANCD2), the underlying mechanism may be similar between ATR and FANCD2. This study extends our understanding of ATR’s role in meiosis, uncovering functions in regulating crossover distribution.
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