The genome stability is maintained by coordinated action of DNA repairs and cell cycle checkpoints. Rad9 is conserved from yeast to human and functions in both DNA lesion repairs and cell cycle checkpoint controls, thus in genomic stabilization. But how exactly Rad9 sense DNA lesions and play roles in DNA repairs and cell cycle controls remain elusive. Recently, Professor Haiying Hang’s laboratory at the Institution of biophysics, Chinese Academy of Sciences has reported that Rad9 interacts with and is methylated by protein arginine methyltransferase 5 (PRMT5). Arginine methylation of Rad9 plays a critical role in S/M and G2/M cell cycle checkpoints. The activation of the Rad9 downstream checkpoint effector Chk1 is impaired in cells expressing a mutant Rad9 that cannot be methylated. Additionally, Rad9 methylation is also required for cellular resistance to DNA damaging stresses. The work was published online in Nucleic Acids Research (February 14, 2011). This paper has been selected by Nucleic Acids Research as a featured article.

Professor Hang’s group had been studying Rad9 for more than eight years. Many research groups including Professor Hang’s group in the past found that Rad9 was phosphorylated at multiple positions on Rad9 protein and these phosphorylations were critical in regulating Rad9 functions in cell cycle controls and DNA repairs. Through this study, Professor Hang’s group has added new insight into the regulation of Rad9 function that methylation and phosphorylation coordinate to modulate Rad9 function.