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ARS Home » Midwest Area » Peoria, Illinois » National Center for Agricultural Utilization Research » Crop Bioprotection Research » Research » Publications at this Location » Publication #199622
Title: The growth inhibitor, furfural, induces cellular stress signals in Saccharomyces cerevisiae

Author
item Gorsich, Steven
item MCCAFFERY, J - JOHNS HOPKNS UNIV,BALT.MD

Submitted to: Meeting Abstract
Publication Type: Abstract Only
Publication Acceptance Date: 7/30/2006
Publication Date: 7/25/2006
Citation: Gorsich, S.W., Mccaffery, J.M. 2006. The growth inhibitor, furfural, induces cellular stress signals in Saccharomyces cerevisiae [abstract]. Yeast Genetics and Molecular Biology Meeting. Paper No. 99C.

Interpretive Summary:

Technical Abstract: Biofuel ethanol as an alternative fuel is gaining interest for environmental and economical reasons. To reach ethanol goals needed in the United States, it will be essential to take advantage of various biomass substrates for ethanol production (e.g., agricultural and industrial waste products). Releasing fermentable sugars from lignocellulosic biomass is often facilitated by treating the biomass with a weak acid. However, breakdown products of xylose and glucose, furfural and 5-hydroxymethylfurfural, are also released which act as growth inhibitors. These inhibitors create an environment that elicits the expression of stress-related genes in Saccharomyces cerevisiae. Recently, 62 S. cerevisiae genes were identified that function during furfural stress tolerance. Yeast mutants lacking these genes failed to grow in furfural's presence, and tolerance to furfural was increased when some of these genes were overexpressed. Several genes from the pentose phosphate pathway (PPP) were among those identified. Since the PPP plays an important role in protecting the cell from various stresses, stress effects in yeast caused by furfural were further investigated. Using various fluorescent indicators and transmission electron microscopy techniques, we determined that furfural causes an increase in reactive oxygen species accumulation, cellular membrane damage (vacuole and mitochondrial membranes), chromatin damage, and cytoskeletal damage in wild-type S. cerevisiae. Whether or not overexpressing any of the previously identified genes will reduce oxidative damage is being investigated.