Poly (ADP-ribose) polymerase-1 (Parp1) is a member of nuclear enzymes family involved in to the response to genotoxic stresses, DNA repair, and is critical for the maintenance of genome stability. During gametogenesis, genome stability is essential for inheritance and formation of healthy gametes. The latter involves DNA double-strand break (DSB)-driven pairing of homologous chromosomes in first meiotic prophase. By analysis of DSB repair kinetics in male meiotic prophase cells of homologous recombination (HR) and nonhomologous end joining (NHEJ)-deficient mouse models, we previously demonstrated an interplay between HR and the conventional NHEJ repair pathway. In the current work, we evaluate the relative contribution of Parp1-dependent NHEJ to the repair of ectopic ionizing radiation (IR)-induced DSBs in control and Parp1-inhibited mouse pachytene spermatocytes before and after the completion of meiotic recombination in stages VI–XI. The disappearance of large, exogenous DSB-related γ-H2AX foci was quantified 1 and 8 h after 1 Gy γ-irradiation of control and 3,4-dihydro-5-[4-(1-piperidinyl)butoxy]-1(2H)quinolinone (DPQ) Parp1-inhibited mice. Late pachytene control spermatocytes obtained 8 h after IR had repaired >80% of DSBs observed at 1 h after IR. However, only 64% of DSBs were repaired in late spermatocytes of DPQ-treated (Parp1-inhibited) mice. Thus, it appears that Parp1 contributes to the repair of a fraction of DSBs in late prophase I, providing further insights in DNA repair pathway choreography during spermatogenic differentiation.

中文翻译：

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Parp1依赖的DNA双链断裂修复在辐射后期粗线精原细胞中。

聚（ADP-核糖）聚合酶-1（Parp1）是核酶家族的成员，参与对基因毒性压力，DNA修复的反应，对维持基因组稳定性至关重要。在配子发生过程中，基因组稳定性对于健康配子的遗传和形成至关重要。后者涉及DNA双链断裂（DSB）驱动的第一个减数分裂前期同源染色体的配对。通过分析同源重组（HR）和非同源末端连接（NHEJ）缺陷小鼠模型的雄性减数分裂前期细胞中DSB修复动力学，我们以前证明了HR和常规NHEJ修复途径之间的相互作用。在目前的工作中，我们评估了在第六至十一阶段减数分裂重组完成之前和之后，对照和Parp1抑制的小鼠粗线精原细胞在异位电离辐射（IR）诱导的DSBs修复中对Parp1依赖性NHEJ的相对贡献。在对对照和3,4-二氢-5- [4-（1-哌啶基）丁氧基] -1（2H）进行1 Gyγ辐照后1和8小时，量化了与DSB相关的大型外源性γ-H2AX病灶的消失。 ）喹啉酮（DPQ）Parp1抑制小鼠。IR后8 h获得的晚期粗线期对照精母细胞修复了IR后1 h观察到的80％以上的DSB。但是，只有64％的DSB在DPQ处理（抑制Parp1的小鼠）的晚期精母细胞中得到修复。因此，似乎Parp1有助于后期前期I修复部分DSB，