Oncoprotein Tudor-SN is a key determinant providing survival advantage under DNA damaging stress.

Xiao Fu, Chunyan Zhang, Hao Meng, Kai Zhang, Lei Shi, Cheng Cao, Ye Wang, Chao Su, Lingbiao Xin, Yuanyuan Ren, Wei Zhang, Xiaoming Sun, Lin Ge, Olli Silvennoinen, Zhi Yao, Xi Yang, Jie Yang

Cell death and differentiation 2018 Sep

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Herein, Tudor-SN was identified as a DNA damage response (DDR)-related protein that plays important roles in the early stage of DDR. X-ray or laser irradiation could evoke the accumulation of Tudor-SN to DNA damage sites in a poly(ADP-ribosyl)ation-dependent manner via interaction with PARP-1. Additionally, we illustrated that the SN domain of Tudor-SN mediated the association of these two proteins. The accumulated Tudor-SN further recruited SMARCA5 (ATP-dependent chromatin remodeller) and GCN5 (histone acetyltransferase) to DNA damage sites, resulting in chromatin relaxation, and consequently activating the ATM kinase and downstream DNA repair signalling pathways to promote cell survival. Consistently, the loss-of-function of Tudor-SN attenuated the enrichment of SMARCA5, GCN5 and acetylation of histone H3 (acH3) at DNA break sites and abolished chromatin relaxation; as a result, the cells exhibited DNA repair and cell survival deficiency. As Tudor-SN protein is highly expressed in different tumours, it is likely to be involved in the radioresistance of cancer treatment.

Citation

Xiao Fu, Chunyan Zhang, Hao Meng, Kai Zhang, Lei Shi, Cheng Cao, Ye Wang, Chao Su, Lingbiao Xin, Yuanyuan Ren, Wei Zhang, Xiaoming Sun, Lin Ge, Olli Silvennoinen, Zhi Yao, Xi Yang, Jie Yang. Oncoprotein Tudor-SN is a key determinant providing survival advantage under DNA damaging stress. Cell death and differentiation. 2018 Sep;25(9):1625-1637