Benjámin R. Baráth1,2 and Laszlo Nagy1,3,4,5 1Department of Biochemistry and Molecular Biology, Faculty of Medicine, University of Debrecen, Debrecen 4032, Hungary; 2Doctoral School of Molecular Cell and Immunobiology, University of Debrecen, Debrecen 4032, Hungary; 3Department of Medicine, Division of Endocrinology, Diabetes, and Metabolism, Johns Hopkins University School of Medicine, Baltimore, Maryland 21224, USA; 4Department of Biological Chemistry, Johns Hopkins University School of Medicine, Baltimore, Maryland 21205, USA; 5Institute for Fundamental Biomedical Research, Johns Hopkins All Children's Hospital, St. Petersburg, Florida 33707, USA Corresponding author: lnagyjhmi.edu Abstract

Metabolic reprogramming of stem cells is a targetable pathway to control regeneration. Activation of stem cells results in down-regulation of oxidative phosphorylation (OXPHOS) and fatty acid oxidation (FAO) and turns on glycolysis to provide fuel for proliferation and specific signaling events. How cell type-specific events are regulated is unknown. In this issue of Genes & Development Ciuffoli and colleagues (pp. 151–167) use metabolomic, gene inactivation, and functional approaches to show that phosphoserine aminotransferase (Psat1), an enzyme in serine biosynthesis, is activated in muscle stem cells and contributes to cell expansion and skeletal muscle regeneration via the production of α-ketoglutarate and glutamine.