The global pathogen Vibrio cholerae monitors environmental polyamines to garner information about numbers of ‘self’ versus ‘other’ in the vicinity, and in response, to remain or disperse from biofilms.

Vibrio cholerae uses a conserved ribosome assembly factor to repress biofilm formation at low temperatures.

Whole-genome sequencing reveals the remarkable extent of horizontally moving genetic material in naturally competent Vibrio cholerae after a prey-killing DNA acquisition process.

The T12 Vibrio cholerae lineage has been continuously circulating in West Africa since at least 2012, highlighting the importance of regional disease control efforts.

Genetic and molecular analyses identify and characterize an evolutionary battle over lysis timing wherein a bacteriophage delays lysis through lysis inhibition while a defensive phage satellite accelerates lysis.

A quorum-sensing-controlled program of multicellularity, aggregation, is identified in Vibrio cholerae, which may be important for transitions between the marine niche and the human host.

Mannose-sensitive hemagglutinin pili act as a braking and anchoring machine during the three-phase landing process of Vibrio cholerae.

Biofilm matrix protein RbmA controls biofilm architecture through binary structural switching and exopolysaccharide binding.

Bacterial viruses are an unexpected ‘third party’ that imposes a strong predatory pressure on a bacterial pathogen during the natural course of infection in humans.

RNA degradation is completed through specific intermediates, such as diribonucleotides, which must be removed from the cells by a specific enzyme.