“Nuclear myosin 1 – from gene to function”

Mitochondria play a vital role in cellular metabolism by generating energy through oxidative phosphorylation (OXPHOS) in most somatic cells. However, highly proliferative, undifferentiated pluripotent stem cells and cancer cells mainly rely on aerobic glycolysis for energy production. Recently, we reported that nuclear myosin 1 (NM1) functions as a tumor suppressor and a key regulator of cellular metabolism, directly controlling the expression of the mitochondrial transcription factors TFAM and Pgc1α. Its deletion alters mitochondrial structure, reduces OXPHOS gene expression, induces a metabolic shift toward aerobic glycolysis, and promotes tumor formation in mice. In this talk, I will move from tumor development to somatic tissues and share our latest findings from phenotyping NM1 knockout mice.