Submitted to: PLoS One
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 10/31/2012
Publication Date: 10/31/2012
Citation: Suo, Y., Huang, Y., Liu, Y., Shi, C., Shi, X. 2012. The expression of superoxide dismutase (SOD) and a putative ABC transporter permease is inversely correlated during biofilm formation in Listeria monocytogenes 4b G. PLoS One. 7:e48467. Interpretive Summary: The bacterium, Listeria monocytogenes, is an important food-borne pathogen that causes disease in humans and animals. L. monocytogenes is difficult to eliminate since it can form a biofilm (a complex aggregation of microorganisms growing on a solid substrate). To understand how biofilms are formed in L. monocytogenes, the gene that encodes for an enzyme known as superoxide dismutase was deleted from the bacterial genome forming what are referred to as mutant strains. Our results showed that these mutant strains grew more slowly and had a decreased capacity for biofilm formation. Information from this study enhances the understanding of the role of superoxide dismutase in L. monocytogenes in biofilm formation and provides information to help in the development intervention strategies.
Technical Abstract: Little is known about the molecular basis of biofilm formation in Listeria monocytogenes. The superoxide dismutase (SOD) of the deletion mutant of lm.G_1771 gene, which encodes for a putative ABC_transporter permease, is highly expressed in biofilm. In this study, the sod gene deletion mutant delta sod, and double deletion mutant of the sod and lm. G_1771 genes delta sod delta 1771 were used to investigate the role of SOD and its relationship to the expression of the putative ABC transporter permease in biofilm formation. Our results showed that the ability of biofilm formation was significantly reduced in the delta sod mutant and the delta 1771 delta sod double mutant. Both delta sod and delta 1771 delta sod mutants exhibited slow growth phenotypes and produced more reactive oxygen species (ROS). The growth was inhibited in the mutants by methyl viologen (MV, internal oxygen radical generator) treatment. In addition, the expression of the oxidation resistance genes (kat), two stress regulators encoding genes (perR and sigB), and one DNA repair gene (recA) were analyzed in both the wild-type L. monocytogenes 4b G and the deletion mutants by RT-qPCR. The expression levels of the four genes were increased in the deletion mutants when biofilms were formed. Taken together, our data indicate that SOD played an important role in biofilm formation through coping with the oxidant burden in deficient antioxidant defenses.