文献类型： 外文期刊

作者： Wang, Xueting ¹ ; Li, Xuemei ¹ ; Li, Duoyun ³ ; Zhang, Yiying ³ ; Bai, Bing ³ ; Chai, Bao ¹ ; Wen, Zewen ³ ;

作者机构： 1.Shenzhen Univ, Shenzhen Nanshan Peoples Hosp, Affiliated Nanshan Hosp, Dept Dermatol, Shenzhen, Peoples R China

2.Guangdong Acad Agr Sci, Vegetable Res Inst, Guangdong Key Lab New Technol Res Vegetables, Guangzhou, Peoples R China

3.Shenzhen Univ, Shenzhen Nanshan Peoples Hosp, Affiliated Nanshan Hosp, Dept Infect Dis, Shenzhen, Peoples R China

4.Shenzhen Univ, Shenzhen Nanshan Peoples Hosp, Shenzhen Key Lab Endogenous Infect, Affiliated Nanshan Hosp, Shenzhen, Peoples R China

关键词： lncRNA; DNA damage response; 5-fluorocytosine; phosphoproteome; YIL163C

期刊名称：FRONTIERS IN MICROBIOLOGY （ 影响因子：4.5； 五年影响因子：5.2 ）

ISSN：

年卷期： 2025 年 16 卷

页码：

收录情况： SCI

摘要： Introduction Long non-coding RNAs (lncRNAs) are increasingly recognized as key regulators in cellular processes, including the DNA damage response (DDR). In Saccharomyces cerevisiae, DDR is critical for maintaining genomic integrity under stress, mediated by proteins like Mec1 and Rad53. However, the involvement of lncRNAs in DDR pathways, remains largely unexplored. This study investigates the function of a novel lncRNA, YIL163C, in promoting cell survival and genomic stability under DNA damage conditions.Methods Genetic suppressor screening was employed to assess the role of YIL163C in rescuing lethality in mec1 Delta sml1 Delta and rad53 Delta sml1 Delta exposed to DNA damage. Proteomic and phosphoproteomic analyses were conducted to evaluate changes in protein abundance and phosphorylation states. The impact of YIL163C on DDR and antifungal drug tolerance, specifically to 5-fluorocytosine, was also examined.Results Overexpression of YIL163C was found to rescue lethality in mec1 Delta sml1 Delta and rad53 Delta sml1 Delta under DNA damage conditions. Proteomic analyses revealed that YIL163C modulates pathways related to DNA replication, ER stress response, and ribosome biogenesis, enhancing cellular resilience to HU-induced stress. Additionally, YIL163C reduced sensitivity to 5-fluorocytosine, indicating a role in antifungal drug tolerance. Phosphoproteomic data suggested YIL163C influences phosphorylation states, potentially acting downstream of the Mec1-Rad53 signaling pathway.Conclusion This study provides new insights into the regulatory mechanisms of lncRNAs in DDR, with broader implications for antifungal therapy and genomic stability research, emphasizing the role of lncRNAs in stress responses beyond traditional protein-centric mechanisms.