Stress signalling articles from across Nature Portfolio

Fibroblasts undergo transient activation into myofibroblasts to restore homeostasis to injured tissues. This Review explores the influence of mechanical cues and epigenetic modifications on (myo)fibroblast activation and memory and discusses potential therapeutic prevention of persistent myofibroblast activation in fibrosis.

The African trypanosome Trypanosoma brucei has been shown to form stress granules in vitro that might be repurposed to enable differentiation and facilitate parasite transmission. Here, Cayla et al. show that differentiation between slender and stumpy forms does involve membrane-less granules that are different from nutritional stress granules.

How growing organs recover from transient injuries is unclear. Here, authors used mouse models of transient cell death in the limb cartilage to identify cellular and molecular mechanisms (e.g. mTORC1) involved in cartilage repair and catch-up growth.

Contact between organelles such as the mitochondria (Mito) and endoplasmic reticulum (ER) is crucial to coordinate vital cellular homeostatic processes. Here we discuss recent work showing that Mito-ER proximity is regulated by heterotypic complexes between the F-actin polymerizing protein Diaphanous-1) and the mitochondrial dynamics protein Mitofusin 2, which confers increased susceptibility to ischemia/reperfusion injury.

The transcriptional coactivators TAZ and YAP pair with transcriptional enhanced associate domains (TEADs) to regulate transcription. TAZ and YAP nuclear condensates ensure optimal transcription. A new study reports that FUS regulates TAZ condensates by maintaining them in a fluid state to drive transcription of target genes.

In nature, organisms constantly face a variety of stresses in the environment. An organism’s ability to resolve a stressful state is crucial in maintaining homeostasis. In this issue of Nature Metabolism, Wei et al. report that redox-dependent caspase cleavage of fatty acid synthase triggers a global cue for stress resolution in Caenorhabditis elegans.

To activate noncanonical LC3B lipidation and NLRP3 inflammasome formation, stimulator of interferon genes (STING) forms a proton channel in Golgi membranes.

Cremer et al. show that the ubiquitin ligase RNF26 and vimentin-based intermediate filaments cooperate to control perinuclear ER membrane organization and thus facilitate recovery from ER stress.