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<p>Living organisms are constantly at the risk of DNA damage caused by factors such as DNA replication errors, reactive oxygen species, and UV radiation. In plants, DNA damage activates the NAC-type transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) that governs DNA damage responses such as cell cycle arrest, stem cell death, and early onset of endoreplication. However, molecular mechanisms underlying the early induction of endoreplication onset in response to DNA damage remain elusive. In this study, we show that CELL CYCLE SWITCH 52 A1 (CCS52A1), an activator of the APC/C E3 ligase, plays a major role in the early onset of endoreplication in response to DNA double-strand breaks (DSBs) in Arabidopsis roots. Upon DSBs, SOG1 directly binds to the <i>CCS52A1</i> locus, thereby inducing its expression. Moreover, early transition to endoreplication in response to DSBs is suppressed in <i>ccs52a1</i> knockout roots. Our data propose that increased polyploidy may function as a unique adaptative mechanism to genotoxic stress in plants.</p>

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SUPPRESOR OF GAMMA RESPONSE 1 promotes early onset of endoreplication upon DNA double-strand breaks by inducing CCS52A1 expression in Arabidopsis roots

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年4月7日

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  • Toshiki Wada,
  • Ayako N. Sakamoto,
  • Masaaki Umeda,
  • Naoki Takahashi

摘要

Living organisms are constantly at the risk of DNA damage caused by factors such as DNA replication errors, reactive oxygen species, and UV radiation. In plants, DNA damage activates the NAC-type transcription factor SUPPRESSOR OF GAMMA RESPONSE 1 (SOG1) that governs DNA damage responses such as cell cycle arrest, stem cell death, and early onset of endoreplication. However, molecular mechanisms underlying the early induction of endoreplication onset in response to DNA damage remain elusive. In this study, we show that CELL CYCLE SWITCH 52 A1 (CCS52A1), an activator of the APC/C E3 ligase, plays a major role in the early onset of endoreplication in response to DNA double-strand breaks (DSBs) in Arabidopsis roots. Upon DSBs, SOG1 directly binds to the CCS52A1 locus, thereby inducing its expression. Moreover, early transition to endoreplication in response to DSBs is suppressed in ccs52a1 knockout roots. Our data propose that increased polyploidy may function as a unique adaptative mechanism to genotoxic stress in plants.