In an advance online publication of Science this week, researchers at the University of Pennsylvania Medical School and their colleagues show that AMP-activated protein kinase — AMPK — "activates stress-promoted transcription via histone H2B phosphorylation." They show that "AMPK recruitment and H2B S36 phosphorylation co-localize within genes activated by AMPK-dependent pathways, and occur both in promoters and transcribed regions." AMPK-dependent H2B S36 phosphorylation, the authors write,