Pseudomonas aeruginosa defends against interbacterial antagonism through the coordinated expression of previously uncharacterized pathways that grant threat-specific protection.

Distinct surfaces of an interbacterial competition cell wall toxin mediate interactions with different cellular binding partners, resulting in an inherent evolutionary trade-off across the toxin superfamily.

Interbacterial interactions can promote mutagenesis, and possibly adaptation, when intoxicated cells survive exposure to type VI secretion-delivered DNA deaminase toxins.

The death of bacterial kin cells releases a danger signal that activates a posttranscriptional response in surviving cells, resulting in the rapid elaboration of interbacterial competition factors.

Diverse LXG toxins delivered by the Esx pathway function as mediators of contact-dependent interbacterial antagonism within and between Gram-positive bacterial species.

Salmonella antibacterial effectors act on Y-shaped DNA substrates resembling replication forks or transcription bubbles and lead to DNA double-strand breaks.

Legionella pneumophila can be inhibited by its own antimicrobial, HGA (homogentisic acid), but its density-dependent resistance to HGA restricts the potential for self-harm.

Capsular polysaccharides of Acinetobacter baumannii regulate type VI secretion system activity, balancing self-protection with interbacterial competitiveness.

Serial cell-to-cell transfer of lipoprotein toxins by outer membrane exchange provides a potent platform for kin discrimination in Myxococcus xanthus.

Genes for adhesion, interbacterial competition, and secondary metabolite production are important colonization factors of the honey bee gut symbiont Frischella perrara and are regulated by the conserved histone-like DNA-binding protein integration host factor.