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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 #191518


item Gorsich, Steven
item Slininger, Patricia - Pat
item Mccaffery, J. Michael

Submitted to: Biotechnology for Fuels and Chemicals Symposium Proceedings
Publication Type: Abstract Only
Publication Acceptance Date: 5/4/2006
Publication Date: 4/30/2006
Citation: Gorsich, S.W., Slininger, P.J., McCaffery, J. 2006. The fermentation inhibitor furfural causes cellular damage to Saccharomyces cerevisiae [abstract]. Biotechnology for Fuels and Chemicals Symposium Proceedings. Paper No. 4-17.

Interpretive Summary:

Technical Abstract: The use of biofuel ethanol is increasingly important for multiple environmental and economical reasons. To reach the United States ethanol goals, it will be essential to take advantage of various biomass substrates for ethanol production. The release of fermentable sugars from lignocellulose biomass for ethanol fermentation is often facilitated by a weak acid hydrolysis step. As a result, inhibitors such as furfural and 5-hydroxymethylfurfural are formed as degradation products of xylose and glucose, respectively. These and other inhibitors present an environment which elicits the expression of stress-related genes in Saccharomyces cerevisiae. Recently, 62 Saccharomyces cerevisiae genes were identified as important in furfural stress tolerance due to the inability of mutants lacking these genes to grow in furfural’s presence. These include some pentose phosphate pathway genes (ZWF1, GND1, RPE1, and TKL1). When some of these genes are overexpressed, we observe an increase in furfural tolerance. 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 actin damage in wild-type Saccharomyces cerevisiae. Whether or not overexpressing any of the previously identified genes will reduce oxidative damage is being investigated.