Polar elongating mycobacteria (Mycobacterium smegmatis) require specific cell wall chemistries, those catalyzed by targets of critical antibiotics, to maintain rod shape at aging sites of the bacillus.

A combined approach of genome sequencing and fluctuation assays shows that antibiotic pressure does not induce adaptive mutations in Mycobacterium smegmatis, supporting drug resistance as a consequence of phenotypic tolerance.

Mutations in several components of a bacterial ribosome are shown to broadly decrease antibiotic and stress sensitivity, and readily accessible reversion mutations allow these ribosomal mutations to serve as stepping stones to high level antibiotic resistance.

Gut microbiota dysbiosis increased Nos2 expression through the 'gut–lung axis', and altered intracellular antimicrobial and anti-inflammatory environment by abnormal NO, ROS, and Defb1, thereby promoting Mycobacteria colonization in mouse lungs.

A newly established reversible model of membrane departitioning and repartitioning in bacteria uncovers the role of a cell wall synthase in regulating membrane partitioning.

The three-dimensional structures of Mycobacterium tuberculosis cytochrome bcc in complex with the antituberculosis agents, Q203 and TB47, explain how these inhibitors suppress activity of the complex.

Functional definition of NrtR and the discovery of its acetylation represents a first paradigm for linking protein acetylation to bacterial central NAD⁺ metabolism.

A high-throughput functional genomics approach combining inducible CRISPR-interference and quantitative imaging yields an atlas of 'phenoprints' to guide gene function assignments, identify metabolic pathway-specific morphotypes, and inform antibiotic mechanism-of-action studies.

The structure of the Mycobacterium smegmatis CIII₂CIV₂ respiratory supercomplex with telacebec (Q203) bound shows how this tuberculosis drug candidate blocks respiration in mycobacteria.