Location: Crop Bioprotection Research
Title: STRESS TOLERANCE IN SACCHAROMYCES CEREVISIAE CELLS OVEREXPRESSING FURFURAL-STRESS GENES Author
Submitted to: Gordon Research Conference Proceedings
Publication Type: Proceedings
Publication Acceptance Date: July 22, 2005
Publication Date: July 17, 2005
Citation: Gorsich, S.W. 2005. Stress tolerance in Saccharomyces cerevisiae cells overexpressing furfural-stress genes [abstract]. Gordon Research Conference Proceedings. Abstract No. 19. Technical Abstract: The release of useable sugars from lignocellulose biomass for industrial ethanol fermentation is facilitated by a weak acid hydrolysis step. As a consequence, inhibitors such as furfural and 5-hydroxymethylfurfural (HMF) are formed as degradation products of xylose and glucose, respectively. Moreover, the fermentative end-product of ethanol is also inhibitory. These inhibitors present an environment which elicits the expression of stress-related genes in Saccharomyces cerevisiae. Recently, 65 S. cerevisiae genes were identified as important in furfural stress tolerance due to the inability of mutants lacking these genes to grow in the presence of furfural. Many of these genes were either previously or subsequently shown to function in response to other stresses (HMF, ethanol, sorbate, osmotic and oxidative). The identified genes represent functions involved in many physiological pathways (metabolism, transcription, translation, budding, organelle maintenance (mitochondria, vacuole, and plasma membrane), and DNA repair and replication), which demonstrates the complexity of this yeast's response to furfural stress. In the present study, we test the importance of many of these genes to furfural stress tolerance. More specifically, genes with a role in metabolism, NADPH/NADH red-ox balance, or known stress responses were overexpressed, and growth was assayed in the presence of furfural, HMF, or ethanol. In addition, since many cellular activities were linked to furfural stress tolerance, we also examined organelle maintenance (mitochondria, vacuole, and peroxisome) in response to furfural exposure.