Radiation induces cell wall remodeling in Saccharomyces cerevisiae, identifying PIR1 as a potential marker

Ionizing radiation is one of the main stressors inducing oxidative stress and genotoxic damage, leading to decreased cellular viability in addition to the activation of various stress response pathways. However, the impact of radiation on fungal cell wall integrity and its associated regulatory network remains poorly understood. The aim of this study was to investigate the effects of X-ray radiation on Saccharomyces cerevisiae on viability and the expression of key cell wall integrity genes. Wild-type Saccharomyces cerevisiae cells were grown to the late logarithmic phase (OD600 = 0.7–0.9) and then were exposed to 0 Gy, 25 Gy, or 50 Gy irradiation. Cell viability was evaluated by spotting and colony-forming unit (CFU) assays. Three independent radiation-related gene expression datasets were retrieved from publicly available databases, and common differentially expressed genes associated with cell wall integrity were determined. Selected targets were validated by real-time quantitative PCR (qPCR). Exposure to both 25 and 50 Gy radiation reduced survival and viability (25 Gy: 85.5 × 104 CFU/mL; 50 Gy: 46.0 × 104 CFU/mL) compared to non-irradiated control cells (103.2 × 104 CFU/mL). The apparent cell wall thickness in the 50 Gy-treated group, measured immediately and 1 hour after irradiation, was reduced compared to the non-irradiated control. A Gene Ontology-based integrative analysis across three independent radiation datasets identified PIR1 as the only shared gene associated with cell wall integrity. Subsequently, qPCR analysis revealed that FKS1 expression remained unchanged, whereas PIR1 expression was reduced in the 50 Gy radiation group compared to the control. These findings support that the ionizing radiation not only affects cellular viability through intracellular damage but also alters cell wall architecture and its regulatory gene networks, potentially increasing susceptibility to irradiation stress.