Fat cells reactivate quiescent neuroblasts via TOR and glial insulin relays in Drosophila.

ABSTRACT: Many stem, progenitor and cancer cells undergo periods of mitotic quiescence from which they can be reactivated. The signals triggering entry into and exit from this reversible dormant state are not well understood. In the developing Drosophila central nervous system, multipotent self-renewing progenitors called neuroblasts undergo quiescence in a stereotypical spatiotemporal pattern. Entry into quiescence is regulated by Hox proteins and an internal neuroblast timer. Exit from quiescence (reactivation) is subject to a nutritional checkpoint requiring dietary amino acids. Organ co-cultures also implicate an unidentified signal from an adipose/hepatic-like tissue called the fat body. Here we provide in vivo evidence that Slimfast amino-acid sensing and Target of rapamycin (TOR) signalling a

SUBMITTER: Sousa-Nunes R 

PROVIDER: S-EPMC3146047 | biostudies-literature | 2011 Mar

REPOSITORIES: biostudies-literature