Loss of the F-ATP synthase c-subunit inhibits a pathological mitochondrial permeability transition pore that is coupled to a maladaptive mitochondrial unfolded protein response while also extending lifespan.
Class-A penicillin-binding proteins are dispensable for rod-like cell-shape but essential for mechanical integrity by sensing and repairing cell-wall defects locally, as investigated in the model system Escherichia coli.
Outer membrane vesicles serve as decoys to reduce the chance of direct polymyxin B (PMB) binding to cells, which partly explains why many clinical isolates and microbial communities can be protected against PMB treatment.
Alteration of host gut microbiota by antibiotic exposure in early life remodeled host intestinal immune development and metabolism and enhanced the induction of type 1 diabetes in genetically predisposed animals.
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.
Conformational flexibility in HIV-1 capsid, provided by cyclophilin A binding, facilitates evasion of capsid-targeting restriction factor MxB, while allowing sequence change to facilitate cytotoxic T-cell evasion.