Nutrient/ TOR signaling controls adipose mitochondrial transcription factor A ( TFAM ) to regulate organismal growth in Droso

Animals must adapt their growth to fluctuations in nutrient availability to ensure proper development. While nutrient‐sensing tissues coordinate organismal growth through interorgan signaling, the metabolic changes within these tissues that mediate whole‐body growth control remain poorly understood. Using Drosophila larvae, we show that TOR (target of rapamycin), a conserved nutrient‐sensing kinase, controls developmental growth through regulation of the mitochondrial genome transcription factor TFAM, which controls mitochondrial bioenergetic capacity. We find that nutrient/TOR signaling post‐transcriptionally suppresses TFAM protein levels. Furthermore, we find that TOR regulation of TFAM in the larval fat body, a key nutrient‐sensing tissue, controls developmental growth. These findings establish a molecular mechanism linking nutrient‐sensing pathways to mitochondrial metabolism, revealing how environmental nutrient availability coordinates organismal growth through tissue‐specific metabolic control.