ArticlePLoS pathogens2023
Divergence of TORC1-mediated stress response leads to novel acquired stress resistance in a pathogenic yeast.
Article in PLoS pathogens, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 5 citations in OpenAlex.
- Twenty-Five Years of the Environmental Stress Response and the Enduring Power of Yeast in Stress Biology.Yeast (Chichester, England) · 2026Review
- The importance of regulated resource reallocation during dynamic environmental shifts in yeast.The EMBO journal · 2026Article
- Regulated resource reallocation is transcriptionally hard wired into the yeast stress response.bioRxiv : the preprint server for biology · 2024Article
- Proxies introduce bias in decoding TORC1 activity.microPublication biology · 2024Article
- The effect of probiotics on select cognitive domains in mild cognitive impairment and Alzheimer's disease: A systematic review and meta-analysis.Journal of Alzheimer's disease reports · 2024Article
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5 authors at 1 institution in 1 country.
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Abstract
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.
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Registered trials
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