Beveridge Ryan D, Staples Christopher J, Patil Abhijit A, Myers Katie N, Maslen Sarah, Skehel J Mark, Boulton Simon J, Collis Spencer J
a Genome Stability Group ; Department of Oncology ; Academic Unit of Molecular Oncology ; University of Sheffield Medical School ; Sheffield , UK.
Cell Cycle. 2014;13(21):3450-9. doi: 10.4161/15384101.2014.956529.
We previously identified and characterized TELO2 as a human protein that facilitates efficient DNA damage response (DDR) signaling. A subsequent yeast 2-hybrid screen identified LARG; Leukemia-Associated Rho Guanine Nucleotide Exchange Factor (also known as Arhgef12), as a potential novel TELO2 interactor. LARG was previously shown to interact with Pericentrin (PCNT), which, like TELO2, is required for efficient replication stress signaling. Here we confirm interactions between LARG, TELO2 and PCNT and show that a sub-set of LARG co-localizes with PCNT at the centrosome. LARG-deficient cells exhibit replication stress signaling defects as evidenced by; supernumerary centrosomes, reduced replication stress-induced γH2AX and RPA nuclear foci formation, and reduced activation of the replication stress signaling effector kinase Chk1 in response to hydroxyurea. As such, LARG-deficient cells are sensitive to replication stress-inducing agents such as hydroxyurea and mitomycin C. Conversely we also show that depletion of TELO2 and the replication stress signaling kinase ATR leads to RhoA signaling defects. These data therefore reveal a level of crosstalk between the RhoA and DDR signaling pathways. Given that mutations in both ATR and PCNT can give rise to the related primordial dwarfism disorders of Seckel Syndrome and Microcephalic osteodysplastic primordial dwarfism type II (MOPDII) respectively, which both exhibit defects in ATR-dependent checkpoint signaling, these data also raise the possibility that mutations in LARG or disruption to RhoA signaling may be contributory factors to the etiology of a sub-set of primordial dwarfism disorders.
我们之前鉴定并表征了TELO2,它是一种促进高效DNA损伤反应(DDR)信号传导的人类蛋白质。随后的酵母双杂交筛选鉴定出LARG;白血病相关的Rho鸟嘌呤核苷酸交换因子(也称为Arhgef12),作为一种潜在的新型TELO2相互作用蛋白。之前已表明LARG与中心体蛋白(PCNT)相互作用,而PCNT与TELO2一样,是高效复制应激信号传导所必需的。在这里,我们证实了LARG、TELO2和PCNT之间的相互作用,并表明LARG的一个亚群与PCNT在中心体共定位。LARG缺陷细胞表现出复制应激信号传导缺陷,表现为:中心体数量过多、复制应激诱导的γH2AX和RPA核灶形成减少,以及对羟基脲反应时复制应激信号传导效应激酶Chk1的激活减少。因此,LARG缺陷细胞对羟基脲和丝裂霉素C等复制应激诱导剂敏感。相反,我们还表明,TELO2和复制应激信号传导激酶ATR的缺失会导致RhoA信号传导缺陷。因此,这些数据揭示了RhoA和DDR信号通路之间的某种程度的串扰。鉴于ATR和PCNT中的突变分别可导致相关的原发性侏儒症疾病——Seckel综合征和II型小头骨发育异常原发性侏儒症(MOPDII),这两种疾病均表现出ATR依赖性检查点信号传导缺陷,这些数据还提出了LARG中的突变或RhoA信号传导破坏可能是一部分原发性侏儒症疾病病因的促成因素的可能性。