Description
Accession Number: GSE45370
Platform:
GPL16244: Agilent-016322 Yeast (V2) Gene Expression 8x15K Microarray (Probe Name version)
Organism: Saccharomyces cerevisiae
Published on 2013-03-22
Summary:
Cells respond to stress and starvation by adjusting their growth rate and enacting stress defense programs. In eukaryotes this involves inactivation of TORC1, which in turn triggers downregulation of ribosome and protein synthesis genes and upregulation of stress response genes. Here we report that the highly conserved inositol pyrophosphate second messengers (including 1-PP-IP5, 5-PP-IP4, and 5-PP-IP5) are also critical regulators of cell growth and the general stress response, acting in parallel to the TORC1 pathway to control the activity of the class I HDAC Rpd3L. In fact, yeast cells that cannot synthesize any of the PP-IPs mount little to no transcriptional response in osmotic, heat, or oxidative stress. Furthermore, PP-IP dependent regulation of Rpd3L occurs independently of the role individual PP-IPs (such as 5-PP-IP5) play in activating specialized stress/starvation response pathways. Thus, the PP-IP second messengers simultaneously activate and tune the global response to stress and starvation signals.
Overall Design:
2-condition experiments. Includes the responses of wild-type (ACY 044) and mutant yeast strains (all are W303 background) to log growth and stress conditions. This series of microarrays were performed on null mutants of various genes in the inositol pyrophosphate synthesis pathway, including several members of the Rpd3L histone deacetylase complex. All mutants were made in W303 strain, MatA yeast, using standard techniques (homologous recombination). Several stress conditions were tested, including heat-shock, oxidative (H2O2), and osmotic stress (0.375M KCl). Cells in mid-log growth were subjected to stress for 20 minutes. In one instance the TOR inhibitor rapamycin was added to determine whether PP-IPs act above/at or below TORC1 in activating the ESR. Taken together, these microarrays show the role of the inositol pyrophosphate synthesis pathway in activating the ESR in stress.
Contact:
Name: jeremy worley
Organization: university of arizona
Laboratory: Capaldi
Deparment: MCB
Address: 1007 e. lowell st. tucson az 85721 USA
Organization: Agilent Technologies
Address: Palo Alto CA 94304 USA
Email: [email protected]
Phone: 877-424-4536
Web-Link: www.agilent.com
Platform:
GPL16244: Agilent-016322 Yeast (V2) Gene Expression 8x15K Microarray (Probe Name version)
Organism: Saccharomyces cerevisiae
Published on 2013-03-22
Summary:
Cells respond to stress and starvation by adjusting their growth rate and enacting stress defense programs. In eukaryotes this involves inactivation of TORC1, which in turn triggers downregulation of ribosome and protein synthesis genes and upregulation of stress response genes. Here we report that the highly conserved inositol pyrophosphate second messengers (including 1-PP-IP5, 5-PP-IP4, and 5-PP-IP5) are also critical regulators of cell growth and the general stress response, acting in parallel to the TORC1 pathway to control the activity of the class I HDAC Rpd3L. In fact, yeast cells that cannot synthesize any of the PP-IPs mount little to no transcriptional response in osmotic, heat, or oxidative stress. Furthermore, PP-IP dependent regulation of Rpd3L occurs independently of the role individual PP-IPs (such as 5-PP-IP5) play in activating specialized stress/starvation response pathways. Thus, the PP-IP second messengers simultaneously activate and tune the global response to stress and starvation signals.
Overall Design:
2-condition experiments. Includes the responses of wild-type (ACY 044) and mutant yeast strains (all are W303 background) to log growth and stress conditions. This series of microarrays were performed on null mutants of various genes in the inositol pyrophosphate synthesis pathway, including several members of the Rpd3L histone deacetylase complex. All mutants were made in W303 strain, MatA yeast, using standard techniques (homologous recombination). Several stress conditions were tested, including heat-shock, oxidative (H2O2), and osmotic stress (0.375M KCl). Cells in mid-log growth were subjected to stress for 20 minutes. In one instance the TOR inhibitor rapamycin was added to determine whether PP-IPs act above/at or below TORC1 in activating the ESR. Taken together, these microarrays show the role of the inositol pyrophosphate synthesis pathway in activating the ESR in stress.
Contact:
Name: jeremy worley
Organization: university of arizona
Laboratory: Capaldi
Deparment: MCB
Address: 1007 e. lowell st. tucson az 85721 USA
Organization: Agilent Technologies
Address: Palo Alto CA 94304 USA
Email: [email protected]
Phone: 877-424-4536
Web-Link: www.agilent.com
| Date made available | 2013 |
|---|---|
| Publisher | Gene Expression Omnibus |