f Avian pathogenic Escherichia coli (APEC) strains cause one of the three most significant infectious diseases in the poultry industry and are also potential food-borne pathogens threating human health. In this study, we showed that ArcA (aerobic respiratory control), a global regulator important for E. coli's adaptation from anaerobic to aerobic conditions and control of that bacterium's enzymatic defenses against reactive oxygen species (ROS), is involved in the virulence of APEC. Deletion of arcA significantly attenuates the virulence of APEC in the duck model. Transcriptome sequencing (RNA-Seq) analyses comparing the APEC wild type and the arcA mutant indicate that ArcA regulates the expression of 129 genes, including genes involved in citrate transport and metabolism, flagellum synthesis, and chemotaxis. Further investigations revealed that citCEFXG contributed to APEC's microaerobic growth at the lag and log phases when cultured in duck serum and that ArcA played a dual role in the control of citrate metabolism and transportation. In addition, deletion of flagellar genes motA and motB and chemotaxis gene cheA significantly attenuated the virulence of APEC, and ArcA was shown to directly regulate the expression of motA, motB, and cheA. The combined results indicate that ArcA controls metabolism, chemotaxis, and motility contributing to the pathogenicity of APEC. Commensal and pathogenic Escherichia coli strains can grow under both aerobic and anaerobic conditions. The enzymes required for catabolism under aerobic versus anaerobic conditions are substantially different, and E. coli has the ability to switch among anaerobic, anaerobic respiratory, and fermentative pathways (1). The expression of genes involved in cellular functions such as nutrient uptake and/or excretion systems, biosynthetic pathways, and macromolecular synthesis are also adjusted in response to oxygen availability (2). The Arc two-component signal transduction system, comprised of the kinase sensor ArcB and its cognate response regulator ArcA, is one of the mechanisms that enable E. coli adaptation to changing oxygen availability (3). Once an environmental signal is received, ArcB undergoes autophosphorylation and catalyzes the transphosphorylation of ArcA, which then promotes or represses expression of Arc-regulated genes. Rather than directly detecting environmental O 2 , ArcB probably senses the redox state of the cell through detection of a reduced electron transport component (4). Under aerobic conditions (5), oxidized forms of quinone electron carriers in the membrane inhibit the autophosphorylation of ArcB, while under anaerobic and microaerobic conditions, ArcB undergoes autophosphorylation. The net activity of ArcB as a kinase for ArcA is expected to progressively increase during the transition from aerobic to anaerobic growth.The ArcA regulon of E. coli K-12 strains has been extensively studied under both aerobic and anaerobic conditions (6, 7). A previous study indicated that about 1,139 genes in the E. coli K-12 genome are regu...
Extraintestinal pathogenic Escherichia coli (ExPEC) is one of the leading causes of bloodstream infections. Characteristically, these organisms exhibit strong resistance to the bactericidal action of host serum. Although numerous serum resistance factors in ExPEC have been identified, their regulatory mechanisms during in vivo infection remain largely unknown. Here, RNA sequencing analyses together with quantitative reverse-transcription PCR revealed that ExPEC genes involved in the biosynthesis of extracytoplasmic polysaccharides (ECPs) including K-capsule, lipopolysaccharide (LPS), colanic acid, peptidoglycan and Yjb exopolysaccharides were significantly upregulated in response to serum under low oxygen conditions and during bloodstream infection. The oxygen sensor FNR directly activated the expression of K-capsule and colanic acid and also indirectly modulated the expression of colanic acid, Yjb exopolysaccharides and peptidoglycan via the known Rcs regulatory system. The global regulator Fur directly or indirectly repressed the expression ofECP biosynthesis genes in iron replete media, whereas the low iron conditions in the bloodstream could relieve Fur repression. Using in vitro and animal models, FNR, Fur and the Rcs system were confirmed as contributing to ExPEC ECP production, serum resistance and virulence. Altogether, these findings indicated that the global regulators FNR andFur and the signaling transduction system Rcs coordinately regulated the expression of ECP biosynthesis genes leading to increased ExPEC serum resistance in response to low oxygen and low iron levels in the bloodstream.
scite is a Brooklyn-based organization that helps researchers better discover and understand research articles through Smart Citations–citations that display the context of the citation and describe whether the article provides supporting or contrasting evidence. scite is used by students and researchers from around the world and is funded in part by the National Science Foundation and the National Institute on Drug Abuse of the National Institutes of Health.
hi@scite.ai
10624 S. Eastern Ave., Ste. A-614
Henderson, NV 89052, USA
Copyright © 2024 scite LLC. All rights reserved.
Made with 💙 for researchers
Part of the Research Solutions Family.