Volume 3 Issue 1, January 2018

Bacterial biofilms fabricate an extracellular amyloid fibre network that intimately links cells together and inhibits the ability of bacteriophages to penetrate the biofilm.

The mechanisms involved in controlling Candida albicans at mucosal sites are not fully understood. Recent work identifies the EphA2 on epithelial cells as a fungal β-glucan receptor that is critical for mediating protective immunity during oral candidiasis.

The development of tools to accelerate identification of causal microorganisms is crucial, and advances in microbial culture, bioinformatics and animal experimentation are currently driving these discoveries.

This Perspective debates the concept of enterotypes and their use to characterize the gut microbiome, and provides a classifier and standardized methodology to aid cross-study comparisons.

To evade autophagy-mediated killing when inside liver cells, the Plasmodium berghei protein UIS3 binds to a key regulator of the autophagy programme, the host protein LC3, and inhibits its interaction with downstream effectors.

At late stages of biofilm development, Escherichia coli cells express the curli polymer CsgA. CsgA assembles into a fibre network that protects biofilms from attack by lytic phages.

Using transcriptome data from marine subsurface sediments, expressed microbial enzymes are shown to be potential targets for secretion by Bacteria, Archaea and Fungi, providing insights into nutrient cycling in the subsurface environment.

Metagenome and genome database analysis based on proteinfamily profiles identifies a diverse group of bacteriophage related to the abundant human gut crAssphage and predicts replication and transcription gene function.

As certain phages can infect some Pseudomonas aeruginosa strains by binding to their pilins, the bacteria have evolved ways to modify these structures via the addition of O-antigen units or polymers of d-arabinofuranose to block phage attachment.

How the oral epithelium discriminates pathogens from commensals is unclear. Ephrin A2 is now shown to bind exposed β-glucans on the surface of the fungal pathogen Candida albicans, which is required to mount a proinflammatory and antifungal response.

Adaptation of the polony method allows numerical abundances of diverse viral groups to be quantified in environmental samples, and reveals that clade B T7-like cyanophages that carry the <Emphasis Type=”Italic”>psbA</Emphasis> gene are more abundant in the Red Sea than clade A phages.

A CRISPR–Cas9-based gene drive array platform is developed and combined with mating-competent Candida albicans haploids to generate homozygous double-deletion mutants, transforming our ability to do genetic interaction analyses in fungi.

Bacillus subtilis cells are able to sense self-produced autoinducers, which gives rise to stronger quorum-sensing-mediated responses, in a process that can influence the generation of persisters during antibiotic treatment.

A widespread anti-phage defence system, DISARM (defence island system associated with restriction–modification), is identified.

Cultivation of a cellulolytic consortium reveals successional community dynamics and the presence of multidomain glycoside hydrolases assembled into stable complexes distinct from cellulosomes, which are produced by a potential pioneer population.

This study reports the viral and cellular N ⁶-methyladenosine (m⁶A) and N ⁶,2′-O-dimethyladenosine (m⁶Am) epitranscriptomes during KSHV latent and lytic infection, and shows that lytic replication induces dynamic epitranscriptome reprogramming of host pathways that control this process.