Influence of furfural on the physiology of Acinetobacter baylyi ADP1.
Acinetobacter
RT-qPCR
acetate metabolism
difurfuryl ether
furfural
lignocellulosic biomass
Journal
FEMS microbiology letters
ISSN: 1574-6968
Titre abrégé: FEMS Microbiol Lett
Pays: England
ID NLM: 7705721
Informations de publication
Date de publication:
29 Jul 2024
29 Jul 2024
Historique:
medline:
30
7
2024
pubmed:
30
7
2024
entrez:
30
7
2024
Statut:
aheadofprint
Résumé
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 NADH-dependent dehydrogenases AreB and FrmA during aerobic acetate catabolism. However, NADH consumption for furfural biotransformation compromises aerobic growth of A. baylyi ADP1. Depending on the growth phase, several 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 NADPH (icd gene) and NADH (sfcA gene) were preferred when furfural was present. Therefore a higher NADH and NADPH production might support furfural biotransformation and biomass production, respectively. In contrast, in the stationary growth phase genes of the glyoxylate shunt were overexpressed probably to save carbon compounds for biomass formation, and only NADH regeneration 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.
Identifiants
pubmed: 39076007
pii: 7723704
doi: 10.1093/femsle/fnae059
pii:
doi:
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM
Informations de copyright
© The Author(s) 2024. Published by Oxford University Press on behalf of FEMS.