Evolution of acquired stress resistance in an opportunistic yeast pathogen

”What does not kill you makes you stronger” has become a well-known modern proverb meaning that one who endures and overcomes a stressful time eventually becomes more resilient and tougher for similar or even more difficult times. A similar phenomenon has been ubiquitously observed in nature in many organisms from single cell organisms like bacteria and fungi, to organisms with more sophisticated structures and systems like mammals. We and other researchers call this phenomenon “acquired stress resistance” (ASR). In ASR, prior experience can influence the organism’s resistance to a future challenge. Currently, most studies are focused on unraveling the molecular mechanism underlying this phenomenon, while much less is known about its emergence and the evolutionary processes that have maintained the key structures while fine-tuning specific features.

To understand the emergence and evolutionary process of ASR, we utilized related yeasts. Yeasts are advantageous in investigating basic biological questions due to their small genome size, short proliferation time, and ease of handling. We have found that the details of ASR diverged between the baker’s yeast and a pathogenic yeast Candida glabrata, which is a common cause of candidiasis in immunocompromised people. Furthermore, we characterized the molecular mechanism underlying the divergence of ASR by examining the behavior of three key proteins: the protein complex hub Target of Rapamycin Complex 1 (TORC1), the signal relay protein and transcription factor Msn4, and the effector protein catalase. Our findings provide the first clear-cut example of ASR divergence. Differences in ASR in different species may relate to their adaptation to their respective natural habitats and impact their pathogenicity and virulence potential.