During development, the progeny of stem cells adopt increasingly restricted fates that must then be maintained, probably through epigenetic mechanisms, to ensure normal development and tissue homeostasis. Hitoshi Sawa and colleagues now reveal the role that the double bromodomain protein BET-1 and the MYST histone acetyltransferases (HATs) play in cell-fate maintenance in C. elegans (see p. ). The researchers show that cells in most bet-1 mutants adopt their correct fate initially but transform later into lineally related cells. By expressing BET-1 at various times during the development of bet-1 mutants, the researchers show that BET-1 functions both when the cell fate of various lineages is acquired to establish a stable fate and at later stages to maintain that fate. Finally, they show that disruption of MYST HATs causes bet-1-like phenotypes, which suggests that BET-1 is recruited to its targets by binding to acetylated histones through its bromodomains. These new insights into cell-fate maintenance might have implications for the treatment of cancer and for the development of cell therapies.
