Title Hrq1 Facilitates Nucleotide Excision Repair of DNA Damage Induced by 4-Nitroquinoline-1-Oxide and Cisplatin in Saccharomyces cerevisiae
Author Do-Hee Choi, Moon-Hee Min, Min-Ji Kim, Rina Lee, Sung-Hun Kwon, and Sung-Ho Bae*
Address Department of Biological Sciences, College of Natural Science, Inha University, Incheon 402-751, Republic of Korea
Bibliography Journal of Microbiology, 52(4),292–298, 2014,
DOI 10.1007/s12275-014-4018-z
Key Words Hrq1, RecQ helicase, DNA helicase, RECQL4 orthologue, nucleotide excision repair, Rad4
Abstract Hrq1 helicase is a novel member of the RecQ family. Among the five human RecQ helicases, Hrq1 is most homologous to RECQL4 and is conserved in fungal genomes. Recent genetic and biochemical studies have shown that it is a functional gene, involved in the maintenance of genome stability. To better define the roles of Hrq1 in yeast cells, we investigated genetic interactions between HRQ1 and several DNA repair genes. Based on DNA damage sensitivities induced by 4-nitroquinoline- 1-oxide (4-NQO) or cisplatin, RAD4 was found to be epistatic to HRQ1. On the other hand, mutant strains defective in either homologous recombination (HR) or postreplication repair (PRR) became more sensitive by additional deletion of HRQ1, indicating that HRQ1 functions in the RAD4-dependent nucleotide excision repair (NER) pathway independent of HR or PRR. In support of this, yeast twohybrid analysis showed that Hrq1 interacted with Rad4, which was enhanced by DNA damage. Overexpression of Hrq1K318A helicase-deficient protein rendered mutant cells more sensitive to 4-NQO and cisplatin, suggesting that helicase activity is required for the proper function of Hrq1 in NER.