| title | author |
|---|---|
Phosphate starvation induced acquired resistance for hydrogen peroxide stress in _C. glabrata_ |
Bin He, Jinye Liang |
We discovered that a relatively short period (45 min) of phosphate starvation increases the resistance of C. glabrata cells to severe (100 mM) hydrogen peroxide by three fold. This acquired resistance effect is stronger with increasing length of phosphate starvation. In the related baker's yeast S. cerevisiae, 45 min of phosphate starvation didn't trigger a protective effect for a lethal dose (10 mM) of hydrogen perxoide. Longer (>90 min) treatment of phosphate starvation did induce mild protection for a lethal dose of H2O2. The cross-stress protection effect is much less than in C. glabrata.
This work is now published on PLoS Pathog 2023 Oct 23;19(10):e1011748. doi: 10.1371/journal.ppat.1011748
Divergence of TORC1-mediated stress response leads to novel acquired stress resistance in a pathogenic yeast
Jinye Liang, Hanxi Tang, Lindsey F. Snyder, Christopher E. Youngstrom, Bin Z. He
PMID: 37871123 PMCID: PMC10621968 DOI: 10.1371/journal.ppat.1011748
Acquired stress resistance (ASR) enables organisms to prepare for environmental changes that occur after an initial stressor. However, the genetic basis for ASR and how the underlying network evolved remain poorly understood. In this study, we discovered that a short phosphate starvation induces oxidative stress response (OSR) genes in the pathogenic yeast C. glabrata and protects it against a severe H2O2 stress; the same treatment, however, provides little benefit in the low pathogenic-potential relative, S. cerevisiae. This ASR involves the same transcription factors (TFs) as the OSR, but with different combinatorial logics. We show that Target-of-Rapamycin Complex 1 (TORC1) is differentially inhibited by phosphate starvation in the two species and contributes to the ASR via its proximal effector, Sch9. Therefore, evolution of the phosphate starvation-induced ASR involves the rewiring of TORC1's response to phosphate limitation and the repurposing of TF-target gene networks for the OSR using new regulatory logics.