Abstract

When hungry, our growling belly reminds us that it is time to eat, and although microbes do not have stomachs, they too must answer the question of how best to ‘feed’ themselves to survive and grow. This themed issue of Trends in Microbiology is devoted to addressing the role of metabolism in microbial life. We are ‘serving up’ a wide range of topics in this issue, ranging from how microbes obtain energy in diverse and sometimes hostile environments to how microbes can alter the metabolism of their host and use host-derived metabolites to their advantage.Our appetizer is a Forum: Science & Society article discussing agents that could promote biofilm disassembly. Consortia of bacteria encased in an extracellular matrix are termed biofilms, and a final step of biofilm growth and development is the release of bacteria from the biofilm to seed new foci of colonization. In particular, signals such as D-amino acids [1xD-amino acids trigger biofilm disassembly. Kolodkin-Gal, I. et al. Science. 2010; 328: 627–629Crossref | PubMed | Scopus (365)See all References][1], rhamnolipids [2xRhamnolipid surfactant production affects biofilm architecture in Pseudomonas aeruginosa PAO1. Davey, M.E. et al. J. Bacteriol. 2003; 185: 1027–1036Crossref | PubMed | Scopus (376)See all References][2] and short-chain fatty acids [3xA fatty acid messenger is responsible for inducing dispersion in microbial biofilms. Davies, D.G. and Marques, C.N. J. Bacteriol. 2009; 191: 1393–1403Crossref | PubMed | Scopus (271)See all References][3] have been found to aid biofilm disassembly. In this article, Romero and Kolter argue that although biofilm disassembly agents are attractive targets to prevent biofilm infections and fouling, economic factors could prevent their development and use.This is followed by the first course, which contains reviews that focus on microbial metabolism and issues related to how bacteria obtain energy, how microbial metabolism can be studied and how it can be altered. Rhee et al. revisit central carbon metabolism in Mycobacterium tuberculosis and detail recent findings regarding its metabolic network. Because carbon metabolism is required for growth, some of the enzymes involved in this could be potential drug targets. Underpinning the work discussed by Rhee et al. are advances in using metabolomics, the analysis of metabolites within a system. Metabolomics has revolutionized the large-scale study of metabolism and Winder et al. review how metabolomics can be performed and applied to study microbial metabolism. Zhang and Keasling review how biosensors of extracellular and intracellular chemicals and metabolites can be constructed during metabolic engineering of microbes. In engineered metabolic systems where microbes are used to produce useful chemicals, microbial metabolism needs to be regulated in order to efficiently produce the desired chemical. Microbes are capable of gathering energy from a diverse range of chemicals beyond carbon, and Bird et al. discuss the bioenergetics of Fe(II)-oxidizing and Fe(III)- reducing bacteria. Bringing us back to pathogenic bacteria, Rohmer et al. discuss how mammals are a rich source of nutrients for pathogenic bacteria. As mammals are not uncolonized and pathogens must compete with commensals for a spot at the mammalian table, metabolic genes could be used by pathogens to allow them to expand into new environments.Once in a host, bacteria and viruses can not only utilize metabolites from within the host, but can also cause an effect on host metabolism. The second course of this issue contains reviews that focus on how microbes can alter host metabolism and use host metabolites. Holmes et al. discuss the metabolic dialog between humans and our gut microbiota. In particular, how metabolites from gut microbiota aid the development of diseases such as inflammatory bowel disease, cancer, diabetes, obesity, cardiovascular dyslipidemia, metabolic endotoxemia and neurological conditions is examined. Yu et al. discuss how human cytomegalovirus increases cellular glucose uptake and glucose metabolism so that the resulting citrate can be used for fatty acid synthesis while maintaining the cellular tricarboxylic acid (TCA) cycle with increased glutamine metabolism. These virally-induced changes to cellular glucose and glutamine utilization are compared to cellular metabolic changes induced by cancer. Finally, Heaton and Randall examine how viruses use and alter host-derived lipids during all stages of the viral life cycle.I hope that you enjoy digging into this issue and I welcome your comments and feedback (etj.tim@elsevier.com). Bon appetit!

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