Abstract
An important prelude to bacterial infection is the ability of a pathogen to survive independently of the host and to withstand environmental stress. The compatible solute trehalose has previously been connected with diverse abiotic stress tolerances, particularly osmotic shock. In this study, we combine molecular biology and biochemistry to dissect the trehalose metabolic network in the opportunistic human pathogen Pseudomonas aeruginosa PAO1 and define its role in abiotic stress protection. We show that trehalose metabolism in PAO1 is integrated with the biosynthesis of branched α-glucan (glycogen), with mutants in either biosynthetic pathway significantly compromised for survival on abiotic surfaces. While both trehalose and α-glucan are important for abiotic stress tolerance, we show they counter distinct stresses. Trehalose is important for the PAO1 osmotic stress response, with trehalose synthesis mutants displaying severely compromised growth in elevated salt conditions. However, trehalose does not contribute directly to the PAO1 desiccation response. Rather, desiccation tolerance is mediated directly by GlgE-derived α-glucan, with deletion of the glgE synthase gene compromising PAO1 survival in low humidity but having little effect on osmotic sensitivity. Desiccation tolerance is independent of trehalose concentration, marking a clear distinction between the roles of these two molecules in mediating responses to abiotic stress.
Highlights
Pseudomonas aeruginosa is a significant human pathogen and one of the most common causes of nosocomial infections [1]
We show that trehalose metabolism in PAO1 is integrated with the biosynthesis of branched α-glucan, with mutants in either biosynthetic pathway significantly compromised for survival on abiotic surfaces
The sugar molecule trehalose is associated with a range of abiotic stress tolerances, osmotic shock
Summary
Pseudomonas aeruginosa is a significant human pathogen and one of the most common causes of nosocomial infections [1]. It is considered a serious medical threat, on a par with methicillin-resistant Staphylococcus aureus and extensively drug-resistant Mycobacterium tuberculosis [2]. P. aeruginosa is an opportunistic pathogen that primarily affects immunocompromised individuals, including patients with immunodeficiencies [3], burn or major injury victims [4] and cannula or catheter implant patients [5]. It is a major pneumonia agent, causing both acute and chronic lung infections. The difficulty of treating established P. aeruginosa infections means that considerable effort is directed towards the prevention of chronic infection in the first place [9]
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