Journal
SCIENTIFIC REPORTS
Volume 11, Issue 1, Pages -Publisher
NATURE PORTFOLIO
DOI: 10.1038/s41598-021-91293-1
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Funding
- Council of Scientific and Industrial Research, Govt. of India [38(1417)/16/EMR-II]
- UGC, Govt. of India [F.30-141/2015 (BSR)]
- SERB, DST, Govt. of India [ECR/2016/000539]
- CSIR, Govt. of India [09/025(0220)/2017-EMRI]
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In plants, the DNA damage response mechanisms play a crucial role in maintaining genome stability by regulating cell cycle progression, repairing DNA damage, and inducing programmed cell death or endoreduplication. ATM and ATR serve as sensor kinases in this process, while the plant-specific transcription factor SOG1 transduces signals from ATM and ATR to regulate key genes involved in cell cycle progression and DNA damage repair under conditions such as high salinity stress. Arabidopsis exposed to high salinity show increased oxidative stress-induced DNA double strand breaks, leading to the induction of endoreduplication, with SOG1 playing a central role in this process.
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.
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