BMC Genomics Research article Comparison of the transcriptomic "stress response" evoked by antimycin A and oxygen deprivation in saccharomyces cerevisiae Liang-Chuan Lai1,4, Matthew T Kissinger2,4, Patricia V Burke3,4 and Kurt E Kwast*4 BioMed Central Open Access Address: 1Department of Physiology, National Taiwan University College of Medicine, Taipei, Taiwan (R.O.C.), 2Coskata Inc., 4575 Weaver Pkwy, Suite 100, Warrenville, IL 60555, USA, 3Department of Microbiology, University of Illinois, Urbana, IL 61801, USA and 4Department of Molecular & Integrative Physiology, University ofIllinois, Urbana, IL 61801, USA Email: Liang-Chuan Lai - llai@ntu.edu.tw; Matthew T Kissinger - mkissi@yahoo.com; Patricia V Burke - burke@life.uiuc.edu; Kurt E Kwast* - kwast@uiuc.edu * Corresponding author Published: 23 December 2008 BMC Genomics 2008, 9:627 doi:10.1186/1471-2164-9-627 This article is available from: http://www.biomedcentral.com/1471-2164/9/627 Received: 22 October 2007 Accepted: 23 December 2008 © 2008 Lai et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. Abstract Background: Acute changes in environmental parameters (e.g., O2, pH, UV, osmolarity, nutrients, etc.) evoke a common transcriptomic response in yeast referred to as the "environmental stress response" (ESR) or "common environmental response" (CER). Why such a diverse array of insults should elicit a common transcriptional response remains enigmatic. Previous functional analyses of the networks involved have found that, in addition to up-regulating those for mitigating the specific stressor, the majority appear to be involved in balancing energetic supply and demand and modulating progression through the cell cycle. Here we compared functional and regulatory aspects of the stress responses elicited by the acute inhibition of respiration with antimycin A and oxygen deprivation under catabolite non-repressed (galactose) conditions. Results: Gene network analyses of the transcriptomic responses revealed both treatments result in the transient (10 – 60 min) down-regulation of MBF- and SBF-regulated networks involved in the G1/S transition of the cell cycle as well as Fhl1 and PAC/RRPE-associated networks involved in energetically costly programs of ribosomal biogenesis and protein synthesis. Simultaneously, Msn2/ 4 networks involved in hexose import/dissimilation, reserve energy regulation, and autophagy were transiently up-regulated. Interestingly, when cells were treated with antimycin A well before experiencing anaerobiosis these networks subsequently failed to respond to oxygen deprivation. These results suggest the transient stress response is elicited by the acute inhibition of respiration and, we postulate, changes in cellular energetics and/or the instantaneous growth rate, not oxygen deprivation per se. After a considerable delay (≥ 1 generation) under anoxia, predictable changes in heme-regulated gene networks (e.g., Hap1, Hap2/3/4/5, Mot3, Rox1 and Upc2) were observed both in the presence and absence of antimycin A. Conclusion: This study not only differentiates between the gene networks that respond to respiratory inhibition and those that respond to oxygen deprivation but suggests the function of the ESR or CER is to balance energetic supply/demand and coordinate growth with the cell cycle, whether in response to perturbations that disrupt catabolic pathways or those that require rapidly up-regulating energetically costly programs for combating specific stressors. Page 1 of 14 (page number not for citation purposes)