Boosting mitochondrial metabolism in neurons in central memory circuits by enhancing Ca2+ retention in the mitochondrial matrix is shown to improve long-term memory formation in flies and mice.

Acetyl-coenzyme A functions as a non-canonical signal to trigger mitophagy, and the acetyl-coenzyme A–NLRX1 axis underlies the KRAS-inhibitor-induced mitophagy response and promotes drug resistance, providing a metabolic mechanism of KRAS inhibitor resistance.

ABSTRACT. First Person is a series of interviews with the first authors of a selection of papers published in Biology Open, helping researchers promote themselves alongside their papers. Kishalay Ghos...