Ser-Gln sites of SOG1 are rapidly hyperphosphorylated in response to DNA double-strand breaks
Ser-Gln sites of SOG1 are rapidly hyperphosphorylated in response to DNA double-strand breaks
复制标题
SOG1 的 Ser-Gln 位点响应 DNA 双链断裂而快速过度磷酸化
DOI：
10.1080/15592324.2018.1477904
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发表时间：
2018
影响因子：
2.9
通讯作者：
Kimura S.
中科院分区：
文献类型：
--
作者：
Yoshiyama K. O.;Kimura S.
DNA损伤反应系统（DDR）是解决DNA双链断裂（DSB）的关键，DSB对基因组完整性构成严重威胁。SOG 1转录因子是拟南芥DDR的主要调节因子。我们以前发现，SOG 1的5个Ser-Gln位点的过度磷酸化是激活DDR的分子开关。在这项研究中，我们确定了SOG 1在DSB诱导处理后20分钟内过度磷酸化，随后激活了几个SOG 1靶基因。使用SOG 1磷酸化突变体，我们证明，虽然过度磷酸化的网站保持不变，随着时间的推移，过度磷酸化的量逐渐增加。这些观察结果表明，快速的SOG 1过度磷酸化受到活性激酶数量的限制。
The DNA damage response system (DDR) is crucial in addressing DNA double-strand breaks (DSBs), which pose a severe threat to genomic integrity. The SOG1 transcription factor is a master regulator of theArabidopsis thalianaDDR. We previously showed that hyperphosphorylation of five Ser-Gln sites of SOG1 is the molecular switch to activate the DDR. In this study, we determined that SOG1 is hyperphosphorylated within 20 minutes following DSB-inducing treatment, followed by activation of several SOG1 target genes. Using SOG1 phosphorylation mutants, we demonstrated that although the hyperphosphorylation sites remain unchanged over time, the amount of hyperphosphorylation gradually increases. These observations suggest that rapid SOG1 hyperphosphorylation is limited by the amount of active kinases.Abbreviations:SOG1, suppressor of gamma response; ATM, Ataxia telangiectasia mutated; ATR, ATM and Rad3-related