Volume 1 Issue 6, June 2016

There are no antibiotic candidates simply waiting to be brought to market. Overcoming the scientific barriers to innovation will require research and coordination beyond anything that exists in academia, industry or government. We discuss a plan to accelerate the discovery of antibiotics and their transition into the clinic.

Human pressures on coral reefs are giving macroalgae a competitive advantage over reef-building corals. These algae support larger, and potentially pathogenic, microbial populations that are metabolically primed for less-efficient, yet faster, carbohydrate remineralization, perpetuating a vicious cycle of reef degradation.

Several microbes produce proteases that cleave antibodies to evade immune recognition. Humans seem to have a receptor on myeloid cells that detects the presence of cleaved antibodies and activates innate immunity.

Antibiotic therapy is a cornerstone of contemporary medicine. Resistance testing is the gold standard for selecting antibiotics, but in some cases they are surprisingly ineffective. A study now shows that pathogens can form a subset of cells which survive, and even continue to grow in the face of antibiotics.

The plant pathogenic fungus Fusarium oxysporum secretes an effector that is similar to a plant peptide hormone, underscoring the variety of mechanisms that plant pathogens have evolved to tamper with host physiology.

Arbuscular mycorrhizal fungi have traditionally been considered an ancient asexual lineage. Comparative genomic analyses of Rhizophagus irregularis provides evidence of sexual reproduction in these fungi.

Genetic evidence demonstrates that some Bathyarchaeota lineages are capable of homoacetogenesis, a metabolism so far restricted to the Bacteria.

The fungal pathogen Fusarium oxysporum is shown to use a functional homologue of the plant regulatory peptide RALF (rapid alkalinization factor) to induce alkalinization and cause disease in plants.

Antibiotic-mediated selection may promote or suppress conjugation dynamics, dependent on the population structure, physiological status of cells and energy availability.

Using a bacteriophage infection model that allows physical separation between growth and mutagenesis, this study provides support for the natural selection of random mutations as a basis for adaptation to stress.

Using Volta phase plate cryo-electron tomography, influenza virus haemagluttinin is shown to induce two independent pathways of viral membrane fusion, through lipidic junctions or through a fusion pore.

Analysis of 60 sites in three ocean basins suggests that overgrowth of fleshy algae on coral reefs supports higher microbial abundances dominated by copiotrophic, potentially pathogenic bacteria via the provision of dissolved inorganic carbon.

The innate immune receptor, LILRA2, specifically senses microbially cleaved host immunoglobulins.

An undetected, phenotypically colistin-resistant subpopulation of Enterobacter cloacae mediates antibiotic treatment failure

Single-cell measurements of metabolic activities using NanoSIMS reveals that substrate limitation increases phenotypic heterogeneity in Klebsiella oxytoca metabolism, which allows cells to cope with nutrient fluctuations.

Antigenic variants from human H1N1 and H3N2 influenza virus libraries possessing random mutations in the haemagglutinin protein, selected by incubation with human and/or ferret convalescent sera, identify escape variants similar to those that have emerged in nature.