The rod cell, a small form of <italic>Candida albicans</italic>, <?A3B2 pi6?>possesses superior fitness to the host gut and adaptation <?A3B2 pi6?>to commensalism

<i>Candida albicans</i> deploys various morphological forms through complex switching mechanisms, ensuring its survival and thriving as a commensal or pathogen in vastly different human niches. In this study, we demonstrate that a novel ''rod'' morphological form of <i>C</i>. <i>albicans</i> coexists and is interchangeable with previously reported white, gray, and opaque forms, constituting a tetra-stable phenotypic switching system. Rod cells arise from the <i>efg1</i> mutant of SC5314 cells or from the clinical BJ1097 strain cultured under glucose-free conditions. They are characterized by a distinct gene expression profile and can be stably maintained through <i>in vitro</i> passaging or <i>in vivo</i> inhabitation of the gastrointestinal (GI) tract of mice. Remarkably, the majority of the <i>efg1</i> mutant cells become rod cells in N-acetylglucosamine (GlcNAc)-containing medium, and the GlcNAc sensor Ngs1 is instrumental in converting the white or gray cells to the rod cells. Conversely, glucose inhibits rod cells through Cph1; consequently, the loss of Cph1 in the <i>efg1</i> mutant cells permits their conversion to rod cells in glucose-replete media. Notably, rod cells of the <i>efg1</i>/ <i>cph1</i> mutant display superior adaptation and longer persistence in the murine GI environment than wild-type white cells. Taken together, these findings establish rod cells as a previously unappreciated form that is not only morphologically and transcriptionally distinguishable but also defined by specific genetic and environmental determinants, shedding light on complex fungus-host interactions.