Nutrient signalling articles from across Nature Portfolio

Enteroendocrine cells in the gut sense food to regulate feeding behavior. Here, the authors show in Drosophila L-glutamate reduces the frequency of calcium oscillations in enteroendocrine cells and decreases the release of NPF, thereby reducing the activation of a pair of anorexic enteric neurons.

Unmet expectations, a previously uncharacterized fly protein, is a SAM sensor for the mTORC1 pathway. Tracing the evolution of Unmet reveals that the pathway uses the GATOR2 complex to capture and repurpose ancestral enzymes as nutrient sensors.

The role of folate metabolism in leukemic stem cells remains understudied. Here, the authors show that inhibition of mitochondrial folate metabolism leads to differentiation of leukemic cells through depletion of purines and suppression of mTORC1.

Kang et al. reveal structural and functional differences in mitochondria across the hepatic lobule. Mitochondrial distinct phosphoproteome influences their functions highlighting how nutrient availability helps to shape mitochondria zonation.

Son et al. show that AMPK- and PP2A-dependent p300 nucleocytoplasmic shuttling regulates mTORC1 activity in response to nutrient status. Models of Hutchinson–Gilford progeria syndrome display increased cytoplasmic p300 and mTORC1 hyperactivation.

Cells use various metabolic pathways to synthesize the building blocks for growth and proliferation. To ensure balanced growth, these biosynthetic processes must be tightly coordinated. We describe a molecular machinery that senses the cellular capacity to make lipids to regulate other biosynthetic processes — such as protein synthesis — accordingly.

Class 3 phosphatidylinositol-3-kinase (PI3K) has a surprising nuclear function as a coactivator of the circadian clock Bmal1–Clock transcription factor complex for rhythmic purine nucleotide metabolism. This finding opens new avenues for establishing the roles of nuclear subunits of class 3 PI3K in metabolic homeostasis.

Both cell cycle arrest and secretions of senescent cells are subject to metabolic control. In this issue of Nature Metabolism, Roh et al. show that lysosomal partitioning of cholesterol potentiates inflammatory secretion during senescence.