The importance of microbial communities (MCs) cannot be overstated. MCs underpin the biogeochemical cycles of the earth’s soil, oceans and the atmosphere, and perform ecosystem functions that impact plants, animals and humans. Yet our ability to predict and manage the function of these highly complex, dynamically changing communities is limited. Building predictive models that link MC composition to function is a key emerging challenge in microbial ecology. Here, we argue that addressing this challenge requires close coordination of experimental data collection and method development with mathematical model building. We discuss specific examples where model–experiment integration has already resulted in important insights into MC function and structure. We also highlight key research questions that still demand better integration of experiments and models. We argue that such integration is needed to achieve significant progress in our understanding of MC dynamics and function, and we make specific practical suggestions as to how this could be achieved.

The H-NS nucleoid-associated DNA-binding protein is an important global repressor of transcription in Gram-negative bacteria. Recently, H-NS has been implicated in the process of xenogeneic silencing, where it represses the transcription of foreign genes acquired by horizontal transfer. This raises interesting questions about the integration of the horizontally acquired genes into the existing gene regulatory networks of the microbe. In particular, how do bacteria derepress silenced genes in order to benefit from their expression without compromising competitive fitness through doing so inappropriately? This article reviews current knowledge about the derepression of genes that are transcriptionally silenced by H-NS. It describes a variety of anti-silencing mechanisms involving (i) protein-independent processes that operate at the level of local DNA structure, (ii) DNA-binding proteins such as Ler, LeuO, RovA, SlyA, VirB, and proteins related to AraC, and (iii) modulatory mechanisms in which H-NS forms heteromeric protein–protein complexes with full-length or partial paralogues such as StpA, Sfh, Hha, YdgT, YmoA or H-NST. The picture that emerges is one of apparently ad hoc solutions to the problem of H-NS-mediated silencing, suggesting that microbes are capable of evolving anti-silencing methods based on the redeployment of existing regulatory proteins rather than employing dedicated, bespoke antagonists. There is also evidence that in a number of cases more sophisticated regulatory processes have been superimposed on these rather simple anti-silencing mechanisms, broadening the range of environmental signals to which H-NS-repressed genes respond.

Exoelectrogenic bacteria are organisms that can transfer electrons to extracellular insoluble electron acceptors and have the potential to be used in devices such as microbial fuel cells (MFCs). Currently, exoelectrogens have been identified in the Alpha -, Beta -, Gamma - and Deltaproteobacteria , as well as in the Firmicutes and Acidobacteria . Here, we describe use of culture-independent methods to identify two members of the genus Arcobacter in the Epsilon p roteobacteria that are selectively enriched in an acetate-fed MFC. One of these organisms, Arcobacter butzleri strain ED-1, associates with the electrode and rapidly generates a strong electronegative potential as a pure culture when it is supplied with acetate. A mixed-community MFC in which ∼90% of the population is comprised of the two Arcobacter species generates a maximal power density of 296 mW/liter. This demonstration of exoelectrogenesis by strain ED-1 is the first time that this property has been shown for members of this genus.

The plasmid‐encoded Per regulatory locus of enteropathogenic Escherichia coli (EPEC) is generally considered to consist of three genes, perA, perB and perC. PerA, a member of the AraC‐like family of transcriptional regulators, is known to be an activator of its own promoter (autoactivation) as well as of the plasmid‐located bfp operon encoding bundle‐forming pili, but its role in activation of the chromosomal locus of enterocyte effacement (LEE) pathogenicity island, which confers the property of intimate adherence on EPEC, requires clarification. Here, we show that PerA is also required for activation of the master regulatory LEE operon, LEE1, but that this activation is indirect, being achieved via autoactivation of the per promoter which ensures sufficient production of the PerC protein to activate LEE1. In contrast, PerA‐dependent activation of the per and bfp promoters is direct and does not require the other Per proteins, but is modulated by the nucleoid‐associated protein H‐NS. The closely related VirF regulator from Shigella flexneri cannot substitute for PerA to activate these promoters, despite being able to bind their upstream regions in vitro. PerA can bind the per and bfp promoter fragments to form multiple complexes, while VirF forms only a single complex. Site‐directed mutagenesis of the PerA protein suggests that, like VirF, it may use both of its carboxy‐terminal helix—turn–helix motifs for DNA interaction, and may also make direct contacts with RNA polymerase. In addition, we have isolated mutations in the poorly characterized amino‐terminal domain of PerA which affect its ability to activate gene expression.