Abstract
ABSTRACTCsrA is a global regulator widespread in bacteria and known to be involved in different physiological processes, including pathogenicity. Deletion of csrA of Acinetobacter baumannii strain ATCC 19606 resulted in a mutant that was unable to utilize a broad range of carbon and energy sources, including amino acids. This defect in amino acid metabolism was most likely responsible for the growth inhibition of the ΔcsrA mutant in human urine, where amino acids are the most abundant carbon source for A. baumannii. Recent studies revealed that deletion of csrA in the A. baumannii strains AB09-003 and ATCC 17961 resulted in an increase in hyperosmotic stress resistance. However, the molecular basis for this observation remained unknown. This study aimed to investigate the role of CsrA in compatible solute synthesis. We observed striking differences in the ability of different A. baumannii strains to cope with hyperosmotic stress. Strains AB09-003 and ATCC 17961 were strongly impaired in hyperosmotic stress resistance in comparison to strain ATCC 19606. These differences were abolished by deletion of csrA and are in line with the ability to synthesize compatible solutes. In the salt-sensitive strains AB09-003 and ATCC 17961, compatible solute synthesis was repressed by CsrA. This impairment is mediated via CsrA and could be overcome by deletion of csrA from the genome.IMPORTANCE The opportunistic human pathogen Acinetobacter baumannii has become one of the leading causes of nosocomial infections around the world due to the increasing prevalence of multidrug-resistant strains and their optimal adaptation to clinical environments and the human host. Recently, it was found that CsrA, a global mRNA binding posttranscriptional regulator, plays a role in osmotic stress adaptation, virulence, and growth on amino acids of A. baumannii AB09-003 and ATCC 17961. Here, we report that this is also the case for A. baumannii ATCC 19606. However, we observed significant differences in the ΔcsrA mutants with respect to osmostress resistance, such as the AB09-003 and 17961 mutants being enhanced in osmostress resistance whereas the ATCC 19606 mutant was not. This suggests that the role of CsrA in osmotic stress adaptation is strain specific. Furthermore, we provide clear evidence that CsrA is essential for growth in human urine and at high temperatures.
Highlights
CsrA is a global regulator widespread in bacteria and known to be involved in different physiological processes, including pathogenicity
A. baumannii strains 17961 and AB09003 did not grow in LB or in tryptone or Müller-Hinton broth, but they used sugars such as arabinose and xylose and the organic acid acetate as carbon sources [41]
A similar observation was made in Escherichia coli, in which CsrA is essential for growth in medium with glycolytic carbon sources but not with pyruvate, which is decarboxylated and fed into the tricarboxylic acid cycle (TCC) [54]
Summary
CsrA is a global regulator widespread in bacteria and known to be involved in different physiological processes, including pathogenicity. Deletion of csrA of Acinetobacter baumannii strain ATCC 19606 resulted in a mutant that was unable to utilize a broad range of carbon and energy sources, including amino acids. Species of the genus Acinetobacter are widespread in nature and found in terrestrial ecosystems, including extreme environments, as well as in animals and humans [1,2,3,4,5,6,7,8] This requires far-reaching adaptations to very different habitats to use different carbon and electron sources, to grow at different physicochemical parameters such as pH and water activity, to adhere and built biofilms on very different substrates, and to combat host defense and antibiotic pressure [2, 3, 9, 10]. The molecular basis of sensing salinity and transmission of the signal to transcription and translation machineries is not understood
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