Stress signalling articles from across Nature Portfolio

The transduction of signals by c-Jun N-terminal kinases (JNK) is highly contextual and has diverse cell functions. Here, the authors reveal tiered kinases in the JNK pathway are regulated by intracellular pH with changed signaling outcomes.

Here, Cornell et al. reveal specific neurotransmitters (gamma-aminobutyric acid and acetylcholine) that regulate the ability of animals to manage metabolic stress through an intestinal acetylcholine receptor.

Dormancy is induced by a cold environment. Here, the authors found that C. elegans undergoes diapause at low temperatures, namely cold-inducible diapause (CID). CID can be induced by the hsf-1 mutation and is regulated by neural pathways and longevity genes.

Zhang et al. illustrate a spatial activation pattern of JNK signaling within the intestinal stem cell lineage and uncover a paracrine JNK-EGFR-JNK feedforward loop that sustains ISC proliferation during stress-induced gut regeneration.

Sensing stress within the endoplasmic reticulum (ER), the ER transmembrane protein IRE1α initiates a signal transduction pathway to restore homeostasis. A study finds that this process requires an ER membrane-bound phase separation event that leads to the local assembly of stress granules (SGs) and delivery of signalling components.

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.