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Regulating Growth versus Stress Defe...
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Kocik, Rachel A.,
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Regulating Growth versus Stress Defense in the Yeast Environmental Stress Response /
Record Type:
Electronic resources : Monograph/item
Title/Author:
Regulating Growth versus Stress Defense in the Yeast Environmental Stress Response // Rachel A Kocik.
Author:
Kocik, Rachel A.,
Description:
1 electronic resource (237 pages)
Notes:
Source: Dissertations Abstracts International, Volume: 86-07, Section: B.
Contained By:
Dissertations Abstracts International86-07B.
Subject:
Genetics. -
Online resource:
https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31769993
ISBN:
9798302170866
Regulating Growth versus Stress Defense in the Yeast Environmental Stress Response /
Kocik, Rachel A.,
Regulating Growth versus Stress Defense in the Yeast Environmental Stress Response /
Rachel A Kocik. - 1 electronic resource (237 pages)
Source: Dissertations Abstracts International, Volume: 86-07, Section: B.
All cells must be able to respond to stressful conditions, including drugs, environmental shifts, mutation, and disease. Activation of a stress response typically requires redirection of cellular resources from growth-promoting processes toward stress defense; however, how cells reallocate resources and which cellular objectives dictate these changes is poorly understood. Budding yeast Saccharomyces cerevisiae is an excellent model to study how cells respond to stress, since many aspects of stress biology are conserved in other organisms. Upon an acute stress, yeast activate a common transcriptomic response known as the environmental stress response (ESR). The ESR includes induced (iESR) genes involved in defense, regulated by transcription factors (TFs) Msn2 and Msn4, and repressed (rESR) genes involved in growth, regulated in part by TF repressors Dot6 and Tod6. Here we investigate the interplay between Msn2/Msn4 and Dot6/Tod6 to understand resource allocation in yeast. We utilized live-cell microscopy imaging to measure activation dynamics of Msn2 and Dot6 along with other single-cell phenotypes such as growth rate, cell size, and cell-cycle phase, before and after salt stress. We found that Msn2 and Dot6 displayed unexpected discordance in their behavior, and that grouping cells based on TF behavior revealed subpopulations of cells with distinct post-stress growth properties. Unexpectedly, increased activation of the Dot6 repressor, which represses growth-promoting genes in the rESR, led to faster post-stress growth rate. Further investigation revealed that loss of Dot6/Tod6 led to slower post-stress growth and a delay in acquiring subsequent stress resistance, while a loss of Msn2/4 led to faster post-stress growth but loss of acquired stress resistance. We propose that rESR repression helps to redirect transcriptional and translational resources to iESR induction. Remarkably, we found that Msn2/4 regulate the abundance and activation of Dot6 and help represses rESR genes. Together this supports a model in which acute stress activates Msn2/4 to induce stress defense genes and aid in repressing rESR genes that are repressed to reallocate resources toward iESR genes, accelerating the acquisition of stress tolerance and enabling cells to respond dynamically to stress.
English
ISBN: 9798302170866Subjects--Topical Terms:
530508
Genetics.
Subjects--Index Terms:
Environmental stress response
Regulating Growth versus Stress Defense in the Yeast Environmental Stress Response /
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All cells must be able to respond to stressful conditions, including drugs, environmental shifts, mutation, and disease. Activation of a stress response typically requires redirection of cellular resources from growth-promoting processes toward stress defense; however, how cells reallocate resources and which cellular objectives dictate these changes is poorly understood. Budding yeast Saccharomyces cerevisiae is an excellent model to study how cells respond to stress, since many aspects of stress biology are conserved in other organisms. Upon an acute stress, yeast activate a common transcriptomic response known as the environmental stress response (ESR). The ESR includes induced (iESR) genes involved in defense, regulated by transcription factors (TFs) Msn2 and Msn4, and repressed (rESR) genes involved in growth, regulated in part by TF repressors Dot6 and Tod6. Here we investigate the interplay between Msn2/Msn4 and Dot6/Tod6 to understand resource allocation in yeast. We utilized live-cell microscopy imaging to measure activation dynamics of Msn2 and Dot6 along with other single-cell phenotypes such as growth rate, cell size, and cell-cycle phase, before and after salt stress. We found that Msn2 and Dot6 displayed unexpected discordance in their behavior, and that grouping cells based on TF behavior revealed subpopulations of cells with distinct post-stress growth properties. Unexpectedly, increased activation of the Dot6 repressor, which represses growth-promoting genes in the rESR, led to faster post-stress growth rate. Further investigation revealed that loss of Dot6/Tod6 led to slower post-stress growth and a delay in acquiring subsequent stress resistance, while a loss of Msn2/4 led to faster post-stress growth but loss of acquired stress resistance. We propose that rESR repression helps to redirect transcriptional and translational resources to iESR induction. Remarkably, we found that Msn2/4 regulate the abundance and activation of Dot6 and help represses rESR genes. Together this supports a model in which acute stress activates Msn2/4 to induce stress defense genes and aid in repressing rESR genes that are repressed to reallocate resources toward iESR genes, accelerating the acquisition of stress tolerance and enabling cells to respond dynamically to stress.
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https://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=31769993
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