The Faculty Research Group of the School of Life Science Continues to Publish Achievements in Scientific Research in Nucleic Acids Research

On October 28, the research group led by Wang Hailong from the School of Life Science published a research paper titled "Human HELQ Regulates DNA End Resection at DNA Double-Strand Breaks and Stalled Replication Forks" online in the international professional journal Nucleic Acids Research in the field of nucleic acid research. 

Nucleic Acids Research is a top journal in the field of biochemistry and molecular biology published by Oxford University Press, with a latest impact factor of 14.9. It mainly publishes cutting-edge research achievements on nucleic acids and proteins related to nucleic acid metabolism. Our university is the first signatory of this paper, Zhao Yuqin and Hou Kaiping, doctoral students studying at the School of Life Science are the co-first authors, and Wang Hailong is the corresponding author. The research work is supported by the National Natural Science Foundation of China and other funds. This paper is an important research achievement published by Wang Hailong's research group again in the journal Nucleic Acid Research after a year.

Correctly repairing DNA double strand break (DSB) and ensuring smooth DNA replication are of great significance for maintaining genome stabilization and avoiding the occurrence of diseases such as tumors. Nuclease-driven DNA end resection occurs both in the early stages of DSB repair and at stalled replication forks under replication pressure. The end resection on DSB is beneficial for homologous recombination (HR) mediated precise DSB repair. However, the end resection on the stalled replication forks can lead to adverse consequences such as instability of the replication forks. Wang Hailong's research team found that HELQ is a new regulatory factor for end resection, which promotes end resection in DSB but inhibits end resection in the stalled replication forks, preventing nuclease from attacking the stalled replication forks (Fig. 1).

This research work for the first time reveals the regulatory function of HELQ in DNA end resection and deeply analyzes its mechanism of action. The research achievements further promote the understanding of the molecular mechanism of DSB resection and replication fork stability maintenance. It is of guiding significance to the analysis of the causes of tumor chemotherapy drug resistance and the design of targeted drugs.