XXXX -Induced Cell Death in @entity5132 and Its Implications for Adaptive Mechanisms of Nutrient Sensing in Yeasts.

@entity1 @entity268 @entity4826 @entity3954 @entity39 @entity26 @entity5132 @entity1919 @entity505
Single-celled organisms have different strategies to sense and utilize nutrients in their ever-changing environments. The opportunistic fungal pathogen @entity5132 is a common member of the @entity1 microbiota, especially that of the gastrointestinal (GI) tract. An important question concerns how @entity5132 gained a competitive advantage over other microbes to become a successful commensal and opportunistic pathogen. Here, we report that @entity5132 uses @entity3954 ( @entity4826 ), an abundant @entity505 source present in the GI tract, as a signal for nutrient availability. When placed in water, @entity5132 cells normally enter the G0 phase and remain viable for weeks. However, they quickly lose viability when cultured in water containing only @entity4826 . We term this phenomenon @entity4826 -induced cell death (GICD). @entity4826 triggers the upregulation of ribosomal biogenesis genes, alterations of mitochondrial metabolism, and the accumulation of reactive @entity26 species (ROS), followed by rapid cell death via both apoptotic and @entity39 mechanisms. Multiple pathways, including the conserved @entity1919 ( @entity268 ) signaling and @entity4826 catabolic pathways, are involved in GICD. @entity4826 acts as a signaling molecule to regulate multiple cellular programs in a coordinated manner and therefore maximizes the efficiency of nutrient use. This adaptive behavior allows @entity5132 ' more efficient colonization of the gut. IMPORTANCE: The ability to rapidly and appropriately respond to nutrients in the environment is crucial to free-living microorganisms. To maximize the use of available nutrients, microorganisms often use a limiting nutritional component as a signal to coordinate multiple biological processes. The @entity1 fungal pathogen @entity5132 uses @entity3954 ( @entity4826 ) as a signal for the availability of external nutrient resources. @entity4826 induces rapid cell death in @entity5132 due to the constitutive activation of oxidative metabolism and accumulation of reactive @entity26 species (ROS), and multiple pathways are involved in its regulation. This study sheds light on the mechanisms of niche specialization of pathogenic fungi and raises the possibility that this cell death pathway could be an unexplored therapeutic target.
