The transcription factor (TF)-binding specificities of Pseudomonas aeruginosa allow us to predict virulence-associated TFs and their target genes, which will facilitate to find effective treatment and prevention for its associated diseases.

Hysteretic switching between virulence states has been observed in a human pathogen.

A response regulator acquired via lateral gene transfer has rewired an ancestral genetic circuitry and regulates alternative pathogenic lifestyles.

M. tuberculosis, the bacterium that causes the disease tuberculosis, uses a signaling system that senses multiple products of the host's immune system to modify gene expression to colonize the lung.

Codon optimization through biased synonymous substitutions is a characteristic feature of the genomes of generalist fungal parasites and is associated with the colonization of multiple hosts.

Conserved transcriptomic profile of uropathogenic E. coli in patients identifies an infection-specific metabolic state.

Fully assembled DNA methylomes from phylogeographically diverse clinical Mycobacterium tuberculosis complex isolates reveals 'intercellular mosaic methylation' as a source of epigenetic diversity.

Cooperation theory and a novel synthetic infection system provides a mechanistic understanding of why a seemingly successful disease management strategy can have devastating consequences for infected hosts.

A phosphorylation circuitry balancing among kinase, transcription factor, transcription repressor, and phosphatase in response against host immunity during M. oryzae–rice interaction.

Feedback from the intestine during infection can modulate the behavior, learning, and microbial perception of the host.