This week’s articles highlight a tRNA synthetase in mTORC1 signaling in fat cell metabolism and aging, the vulnerability of cancer cells to drugs that target proteostasis, and a mechanism by which stressed neurons expel protein aggregates and dysfunctional organelles.
METABOLISM
Promoting adiposity and aging
Arif et al. report that mTORC1 signals through a tRNA synthetase that binds to a lipid transporter to promote lipid uptake by adipocytes and aging in mice (see also Selman and Withers).
CANCER
Targeting proteostasis in pancreatic cancer
Genovese et al. found that the metabolic reprogramming that enables pancreatic cancer cells to escape dependence on oncogenic Kras signaling also sensitizes the cells to drugs that interfere with proteostasis.
NEUROSCIENCE
Neuronal release of aggregated proteins and dysfunctional mitochondria
Melentijevic et al. demonstrate that neurotoxic stress causes C. elegans neurons to expel protein aggregates and dysfunctional mitochondria, a phenomenon that could contribute to the cell-to-cell transmission of neurodegenerative pathology.