Center for Experimental BioInformatics, Department of Biochemistry and Molecular Biology, University of Southern Denmark, Campusvej 55, DK-5230 Odense M, Denmark.
Mol Cell Proteomics. 2010 Jun;9(6):1314-23. doi: 10.1074/mcp.M900616-MCP200. Epub 2010 Feb 16.
To investigate the temporal regulation of the DNA damage response, we applied quantitative mass spectrometry-based proteomics to measure site-specific phosphorylation changes of nuclear proteins after ionizing radiation. We profiled 5204 phosphorylation sites at five time points following DNA damage of which 594 sites on 209 proteins were observed to be regulated more than 2-fold. Of the 594 sites, 372 are novel phosphorylation sites primarily of nuclear origin. The 594 sites could be classified to distinct temporal profiles. Sites regulated shortly after radiation were enriched in the ataxia telangiectasia mutated (ATM) kinase SQ consensus sequence motif and a novel SXXQ motif. Importantly, in addition to induced phosphorylation, we identified a considerable group of sites that undergo DNA damage-induced dephosphorylation. Together, our data extend the number of known phosphorylation sites regulated by DNA damage, provides so far unprecedented temporal dissection of DNA damage-modified phosphorylation events, and elucidate the cross-talk between different types of post-translational modifications in the dynamic regulation of a multifaceted DNA damage response.
为了研究 DNA 损伤反应的时相调控,我们应用基于定量质谱的蛋白质组学方法,在电离辐射后测量核蛋白的特定部位磷酸化变化。我们在 DNA 损伤后的五个时间点对 5204 个磷酸化位点进行了分析,其中 209 个蛋白上的 594 个位点被观察到发生了 2 倍以上的调节。在这 594 个位点中,有 372 个是新的磷酸化位点,主要来源于核。这 594 个位点可以分为不同的时相特征。在辐射后短时间内被调节的位点富含共济失调毛细血管扩张突变(ATM)激酶 SQ 基序和一个新的 SXXQ 基序。重要的是,除了诱导的磷酸化,我们还鉴定了相当数量的经历 DNA 损伤诱导去磷酸化的位点。总之,我们的数据扩展了已知受 DNA 损伤调控的磷酸化位点的数量,提供了迄今为止对 DNA 损伤修饰的磷酸化事件前所未有的时间剖析,并阐明了不同类型的翻译后修饰之间的相互作用在多方面的 DNA 损伤反应的动态调控中的作用。