Influence of furfural on the physiology of Acinetobacter baylyi ADP1

Abstract

Pretreatment of lignocellulosic biomass produces growth inhibitory substances such as furfural which is toxic to microorganisms. Acinetobacter baylyi ADP1 cannot use furfural as a carbon source , instead it biotransforms this compound into difurfuryl ether using the reduced nicotinamide adenine dinucleotide (NADH)-dependent dehydrogenases AreB and FrmA during aerobic acetate catabolism. How ever, N ADH consumption for furfural biotransformation compromises aerobic growth of A. baylyi ADP1. Depending on the growth phase , sever al genes related to acetate catabolism and oxidative phosphorylation changed their expression indicating that central metabolic pathways were affected by the presence of furfural. During the exponential growth phase, reactions involved in the formation of reduced nicotinamide adenine dinucleotide phosphate (NADPH) ( icd gene) and N ADH ( sfcA gene) were preferred when furfural was present. Therefore a higher N ADH and N ADPH production might support furfural biotransformation and biomass production, respectively. In contrast, in the stationar y growth phase genes of the glyoxylate shunt were over expressed probably to save carbon compounds for biomass formation, and only N ADH re generation was appreciated. Finally, disruption of the frmA or areB gene in A. baylyi ADP1 led to a decrease in growth adaptation and in the capacity to biotransform furfural. The characterization of this physiological behavior clarifies the impact of furfural in Acinetobacter metabolism.