Jinye Liang
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Jinye Liang has a total of 4 co-authors. Here are the top co-authors by number of shared publications:
- Bin Z. He
Department of Biology, University of Iowa
2 shared publications Christopher E. Youngstrom
Affiliation Department of Biology, The University of Iowa, Iowa City, Iowa, United States of America
2 shared publicationsHanxi Tang
Affiliation Department of Biology, The University of Iowa, Iowa City, Iowa, United States of America
2 shared publicationsLindsey F. Snyder
Affiliation Interdisciplinary Graduate Program in Genetics, The University of Iowa, Iowa City, Iowa, United States of America
2 shared publications
Latest Publications
- Open Access
- 23 October 2023
- Published by Public Library of Science (PLoS) in PLOS Pathogens
- Vol. 19 (10) , e1011748
Divergence of TORC1-mediated stress response leads to novel acquired stress resistance in a pathogenic yeast
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.
- 23 October 2023
- Published by Public Library of Science (PLoS) in PLOS Pathogens
- Vol. 19 (10) , e1011748
Open AccessDivergence of TORC1-mediated stress response leads to novel acquired stress resistance in a pathogenic yeast
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.
- Open Access
Divergence of TORC1-mediated Stress Response Leads to Novel Acquired Stress Resistance in a Pathogenic Yeast
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 H 2 O 2 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.
Open AccessDivergence of TORC1-mediated Stress Response Leads to Novel Acquired Stress Resistance in a Pathogenic Yeast
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 H 2 O 2 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.