Nucleotide Excision Repair Protein Rad23 Regulates Cell Virulence Independent of Rad4 in Candida albicans.

In the pathogenic yeast , the DNA damage response contributes to pathogenicity by regulating cell morphology transitions and maintaining survival in response to DNA damage induced by reactive oxygen species (ROS) in host cells. However, the function of nucleotide excision repair (NER) in has not been extensively investigated. To better understand the DNA damage response and its role in virulence, we studied the function of the Rad23 nucleotide excision repair protein in detail. The deletion strain and overexpression strain both exhibit UV sensitivity, confirming the critical role of in the nucleotide excision repair pathway. Genetic interaction assays revealed that the role of in the UV response relies on but is independent of , , and and have similar roles in regulating cell morphogenesis and biofilm formation; however, only , but not , plays a negative role in virulence regulation in a mouse model. We found that the deletion strain showed decreased survival in a -macrophage interaction assay. Transcriptome sequencing (RNA-seq) and quantitative real-time PCR (qRT-PCR) data further revealed that , but not , regulates the transcription of a virulence factor, , suggesting a unique role of in virulence regulation. Taking these observations together, our work reveals that the -related nucleotide excision pathway plays a critical role in the UV response but may not play a direct role in virulence. The virulence-related role of may rely on the regulation of several virulence factors, which may give us further understanding about the linkage between DNA damage repair and virulence regulation in remains a significant threat to the lives of immunocompromised people. An understanding of the virulence and infection ability of cells in the mammalian host may help with clinical treatment and drug discovery. The DNA damage response pathway is closely related to morphology regulation and virulence, as well as the ability to survive in host cells. In this study, we checked the role of the nucleotide excision repair (NER) pathway, the key repair system that functions to remove a large variety of DNA lesions such as those caused by UV light, but whose function has not been well studied in We found that Rad23, but not Rad4, plays a role in virulence that appears independent of the function of the NER pathway. Our research revealed that the NER pathway represented by Rad4/Rad23 may not play a direct role in virulence but that Rad23 may play a unique role in regulating the transcription of virulence genes that may contribute to the virulence of .