ADP-ribosylation of proteins is crucial for fundamental cellular processes. Despite increasing examples of DNA ADP-ribosylation, the impact of this modification on DNA metabolism and cell physiology is unknown. Here, we show that the DarTG toxin-antitoxin system from enteropathogenic Escherichia coli (EPEC) catalyzes reversible ADP-ribosylation of single-stranded DNA (ssDNA). The DarT toxin recognizes specific sequence motifs. EPEC DarG abrogates DarT toxicity by two distinct mechanisms: removal of DNA ADP-ribose (ADPr) groups and DarT sequestration. Furthermore, we investigate how cells recognize and deal with DNA ADP-ribosylation. We demonstrate that DNA ADPr stalls replication and is perceived as DNA damage. Removal of ADPr from DNA requires the sequential activity of two DNA repair pathways, with RecF-mediated homologous recombination likely to transfer ADP-ribosylation from single-to double-stranded DNA (dsDNA) and subsequent nucleotide excision repair eliminating the lesion. Our work demonstrates that these DNA repair pathways prevent the genotoxic effects of DNA ADP-ribosylation.

Accurate assessment of the antibacterial activity of graphene requires consideration of both the graphene fabrication method and, for supported films, the properties of the substrate.Large-area graphene films produced by chemical vapor deposition were grown directly on copper substrates or transferred on a gold substrate and their effect on the viability and proliferation of the Gram-positive bacteria Staphylococcus aureus and the Gram-negative bacteria Escherichia coli were assessed. The viability and the proliferation of both bacterial species were not affected when they were grown on a graphene film entirely covering the gold substrate, indicating that conductivity plays no role on bacterial viability and graphene has no antibacterial activity against S. aureus and E. coli. On the other hand, antibacterial activity * Corresponding author : Email address : louis.dellieu@unamur.be (L. Dellieu) FAX : +32 81 72 44 64 2 was observed when graphene coated the copper substrates, resulting from the release of bactericidal cupric ions in inverse proportion to the graphene surface coverage.

The interactions between microbes and their hosts are among the most complex biological phenomena known today. The interaction may reach from overall beneficial interaction, as observed for most microbiome/microbiota related interactions to interaction with virulent pathogens, against which host cells have evolved sophisticated defence strategies. Among the latter, the confinement of invading pathogens in a phagosome plays a key role, which often results in the destruction of the invader, whereas some pathogens may counteract phagosomal arrest and survive by gaining access to the cytosol of the host cell. In the current review, we will discuss recent insights into this dynamic process of host-pathogen interaction, using Mycobacterium tuberculosis and related pathogenic mycobacteria as main examples. | INTRODUCTIONIn this review dedicated to recent research on bacteria-induced phagosomal rupture, our discussion will mainly focus on Mycobacterium tuberculosis (Mtb), the causative agent of human tuberculosis (TB). This key human pathogen was only relatively recently counted among the pathogens that have the ability to rupture the phagosome and egress to the cytosol of host phagocytes. A short comparative analysis of Mtb with selected classical cytosolic pathogens of other bacterial phyla will complete the presented perspectives.

Stress response to fluctuating environments often implies a time-consuming reprogramming of gene expression. In bacteria, the so-called bet hedging strategy, which promotes phenotypic stochasticity within a cell population, is the only fast stress response described so far(1). Here, we show that Caulobacter crescentus asymmetrical cell division allows an immediate bimodal response to a toxic metals-rich environment by allocating specific defence strategies to morphologically and functionally distinct siblings. In this context, a motile swarmer cell favours negative chemotaxis to flee from a copper source, whereas a sessile stalked sibling engages a ready-to-use PcoAB copper homeostasis system, providing evidence of a prompt stress response through intrinsic bacterial dimorphism.