Hyperacute response proteins synthesized on γ-tubulin-FTO-MARK4 translation microdomains regulate cancer’s acute stress response
Saleme et al. show that cancer’s stress resistance is driven by translation of hyperacute response proteins from m6A-tagged mRNAs within minutes of various stresses (metabolic stress, radiation, oxidative stress, or chemotherapy). Translation is mediated by cytosolic FTO activation by MARK4 on specialized γ-tubulin-associated ribosomes. FTO and MARK4 inhibitors are therapeutic targets for cancer’s resistance to stress.
