Hrq1 facilitates nucleotide excision repair of DNA damage induced by 4-nitroquinoline-1-oxide and cisplatin in Saccharomyces cerevisiae.

作者: Do-Hee Choi , Moon-Hee Min , Min-Ji Kim , Rina Lee , Sung-Hun Kwon

DOI: 10.1007/S12275-014-4018-Z

关键词:

摘要: Hrq1 helicase is a novel member of the RecQ family. Among five human helicases, most homologous to RECQL4 and conserved in fungal genomes. Recent genetic biochemical studies have shown that it functional gene, involved maintenance genome stability. To better define roles yeast cells, we investigated interactions between HRQ1 several DNA repair genes. Based on damage sensitivities induced by 4-nitroquinoline-1-oxide (4-NQO) or cisplatin, RAD4 was found be epistatic HRQ1. On other hand, mutant strains defective either recombination (HR) post-replication (PRR) became more sensitive additional deletion HRQ1, indicating functions RAD4-dependent nucleotide excision (NER) pathway independent HR PRR. In support this, two-hybrid analysis showed interacted with Rad4, which enhanced damage. Overexpression Hrq1K318A helicase-deficient protein rendered cells 4-NQO suggesting activity required for proper function NER.

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