Shah Govind A, O'Shea Clodagh C
Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.
Molecular and Cell Biology Laboratory, Salk Institute for Biological Studies, 10010 North Torrey Pines Road, La Jolla, CA 92037-1002, USA.
Cell. 2015 Aug 27;162(5):987-1002. doi: 10.1016/j.cell.2015.07.058.
In response to cellular genome breaks, MRE11/RAD50/NBS1 (MRN) activates a global ATM DNA damage response (DDR) that prevents cellular replication. Here, we show that MRN-ATM also has critical functions in defending the cell against DNA viruses. We reveal temporally distinct responses to adenovirus genomes: a critical MRN-ATM DDR that must be inactivated by E1B-55K/E4-ORF3 viral oncoproteins and a global MRN-independent ATM DDR to viral nuclear domains that does not impact viral replication. We show that MRN binds to adenovirus genomes and activates a localized ATM response that specifically prevents viral DNA replication. In contrast to chromosomal breaks, ATM activation is not amplified by H2AX across megabases of chromatin to induce global signaling and replicative arrest. Thus, γH2AX foci discriminate "self" and "non-self" genomes and determine whether a localized anti-viral or global ATM response is appropriate. This provides an elegant mechanism to neutralize viral genomes without jeopardizing cellular viability.
针对细胞基因组断裂,MRE11/RAD50/NBS1(MRN)激活一种全局性的ATM DNA损伤反应(DDR),从而阻止细胞复制。在此,我们表明MRN-ATM在保护细胞抵御DNA病毒方面也具有关键功能。我们揭示了对腺病毒基因组在时间上不同的反应:一种关键的MRN-ATM DDR,必须被E1B-55K/E4-ORF3病毒癌蛋白灭活,以及一种全局性的不依赖MRN的针对病毒核结构域的ATM DDR,其不影响病毒复制。我们表明MRN与腺病毒基因组结合并激活一种局部性的ATM反应,该反应特异性地阻止病毒DNA复制。与染色体断裂不同,ATM的激活不会通过H2AX在数百万碱基对的染色质上进行放大以诱导全局性信号传导和复制停滞。因此,γH2AX焦点区分“自身”和“非自身”基因组,并确定局部抗病毒反应还是全局性ATM反应是合适的。这提供了一种巧妙的机制来中和病毒基因组而不危及细胞活力。