| Summary: | <i>Candida albicans</i> displays the ability to adapt to a wide variety of environmental conditions, triggering signaling pathways and transcriptional regulation. Sko1 is a transcription factor that was previously involved in early hypoxic response, cell wall remodeling, and stress response. In the present work, the role of <i>sko1</i> mutant in <i>in viv</i>o and <i>ex vivo</i> studies was explored. The <i>sko1</i> mutant behaved as its parental wild type strain regarding the ability to colonize murine intestinal tract, <i>ex vivo</i> adhesion to murine gut epithelium, or systemic virulence. These observations suggest that Sko1 is expendable during commensalism or pathogenesis. Nevertheless, the study of the <i>hog1 sko1</i> double mutant showed unexpected phenotypes. Previous researches reported that the deletion of the <i>HOG1</i> gene led to avirulent <i>C. albicans</i> mutant cell, which was, therefore, unable to establish as a commensal in a gastrointestinal murine model. Here, we show that the deletion of <i>sko1</i> in a <i>hog1</i> background reverted the virulence of the <i>hog1</i> mutant in a systemic infection model in <i>Galleria mellonella</i> larvae and slightly improved the ability to colonize the murine gut in a commensalism animal model compared to the <i>hog1</i> mutant. These results indicate that Sko1 acts as a repressor of virulence related genes, concluding that Sko1 plays a relevant role during commensalism and systemic infection.
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