Department of Botany, UGC Center for Advanced Studies, The University of Burdwan, Golapbag Campus, Burdwan, West Bengal, 713 104, India.
Sci Rep. 2021 Jun 2;11(1):11659. doi: 10.1038/s41598-021-91293-1.
As like in mammalian system, the DNA damage responsive cell cycle checkpoint functions play crucial role for maintenance of genome stability in plants through repairing of damages in DNA and induction of programmed cell death or endoreduplication by extensive regulation of progression of cell cycle. ATM and ATR (ATAXIA-TELANGIECTASIA-MUTATED and -RAD3-RELATED) function as sensor kinases and play key role in the transmission of DNA damage signals to the downstream components of cell cycle regulatory network. The plant-specific NAC domain family transcription factor SOG1 (SUPPRESSOR OF GAMMA RESPONSE 1) plays crucial role in transducing signals from both ATM and ATR in presence of double strand breaks (DSBs) in the genome and found to play crucial role in the regulation of key genes involved in cell cycle progression, DNA damage repair, endoreduplication and programmed cell death. Here we report that Arabidopsis exposed to high salinity shows generation of oxidative stress induced DSBs along with the concomitant induction of endoreduplication, displaying increased cell size and DNA ploidy level without any change in chromosome number. These responses were significantly prominent in SOG1 overexpression line than wild-type Arabidopsis, while sog1 mutant lines showed much compromised induction of endoreduplication under salinity stress. We have found that both ATM-SOG1 and ATR-SOG1 pathways are involved in the salinity mediated induction of endoreduplication. SOG1was found to promote G2-M phase arrest in Arabidopsis under salinity stress by downregulating the expression of the key cell cycle regulators, including CDKB1;1, CDKB2;1, and CYCB1;1, while upregulating the expression of WEE1 kinase, CCS52A and E2Fa, which act as important regulators for induction of endoreduplication. Our results suggest that Arabidopsis undergoes endoreduplicative cycle in response to salinity induced DSBs, showcasing an adaptive response in plants under salinity stress.
如同在哺乳动物系统中一样，DNA 损伤响应细胞周期检查点功能通过广泛调节细胞周期的进程，在修复 DNA 损伤和诱导程序性细胞死亡或内复制，从而在维持基因组稳定性方面发挥着关键作用。ATM 和 ATR（共济失调-毛细血管扩张症突变和 RAD3 相关）作为传感器激酶发挥作用，在将 DNA 损伤信号传递到细胞周期调控网络的下游元件中发挥关键作用。植物特异性 NAC 结构域家族转录因子 SOG1（γ反应抑制物 1 的抑制物）在基因组双链断裂（DSBs）存在的情况下，在从 ATM 和 ATR 传递信号方面发挥着关键作用，并被发现在调节参与细胞周期进程、DNA 损伤修复、内复制和程序性细胞死亡的关键基因方面发挥着关键作用。在这里，我们报告说，暴露在高盐度下的拟南芥会产生氧化应激诱导的 DSBs，同时伴随着内复制的诱导，表现出细胞体积增大和 DNA 倍性水平升高，而染色体数目没有任何变化。在 SOG1 过表达系中，这些反应比野生型拟南芥更为显著，而 sog1 突变系在盐胁迫下内复制的诱导作用明显受损。我们发现，ATM-SOG1 和 ATR-SOG1 途径都参与了盐介导的内复制诱导。SOG1 通过下调关键细胞周期调节剂的表达，包括 CDKB1;1、CDKB2;1 和 CYCB1;1，同时上调 WEE1 激酶、CCS52A 和 E2Fa 的表达，从而促进拟南芥在盐胁迫下的 G2-M 期停滞，后者作为诱导内复制的重要调节剂。我们的结果表明，拟南芥对盐诱导的 DSBs 作出内复制周期反应，在植物应对盐胁迫时展示出适应性反应。
