Atrophic muscles of patients and animal models developing amyotrophic lateral sclerosis show an upregulation of TAp63 that stimulates the expression of a pro-atrophic ubiquitin ligase.

The helical cell shape of Helicobacter pylori depends on the polymerizing cytoskeletal protein CcmA’s recruitment to the cell envelope by Csd5 and CcmA’s indirect stabilization of a periplasmic cell wall hydrolase via interactions with the transmembrane protein Csd7.

Peptidoglycan precursor synthesis occurs in both growing and non-growing regions of the mycobacterial cell surface.

Muscle hypertrophy and regeneration are critically regulated by combination of TGF-β type I receptors in myofibres.

Gut microbiota reshaped by myostatin gene variation has a positive effect on skeletal muscle growth by activating GPR43 through valeric acid, as a metabolite of gut microbiota.

Evolutionary loss of foot muscle in a bipedal rodent shares similarities with skeletal muscle atrophy, which is typically considered a pathological response to injury or disease.

The helical bacterium Helicobacter pylori patterns cell wall synthesis using two distinct cytoskeletal proteins, CcmA and MreB, to achieve its characteristic shape.

Newly prepared double gene-edited sheep provide excellent models for skeletal muscle growth and development, and muscle diseases such as muscle atrophy and sarcopenia.

The prokaryotic actin homologue MreB forms antiparallel double filaments in vitro and in vivo, an architecture that is unprecedented among the actin family of proteins.

Labeling with ¹³C and ¹⁵N in the absence of metabolic engineering enabled the exploration of peptidoglycan metabolism at a very fine level of detail based on kinetic characterization of isotopologues predicted to occur according to known recycling and biosynthesis pathways.