Meeting Abstract

P1.7  Jan. 4  Ecdysone signaling controls fat-body remodeling during metamorphosis in Drosophila melanogaster BOND, N; HOSHIZAKI, DK*; Univ. of Nevada Las Vegas; Univ. of Nevada Las Vegas dkhosh@clark.nscee.edu

The major signal for entry into metamorphosis is a high-titer pulse of the steroid hormone 20-hydroxy-ecdysone (herein referred to as Ecdysone) which triggers the induction of growth and differentiation of adult tissues, and the activation of autophagy and cell death of obsolete larval tissues. The larval fat body, however, is refractive to Ecdysone-induced cell death. Moreover, energy stored in the fat cells is used to fuel the re-architecture of the larva to the adult form. We report that the larval fat body is responsive to Ecdysone and undergoes tissue remodeling leading to the dissociation of the fat body and release of individual cells. We demonstrate by genetic analysis that both partners of the canonical Ecdysone Receptor, EcR and USP, are necessary for fat-body dissociation. Because inactivation of the Receptor also leads to pupal lethality, Ecdysone might also modulate the release of fat cell energy stores. We demonstrate that the regulatory gene ßFtz-F1 is necessary for dissociation of the fat body. Furthermore, the premature expression of ßFtz-F1 is sufficient to induce precocious fat-body dissociation in vivo. ßFtz-F1 is transcriptionally activated in response to the decline in the Ecdysone titer that triggers metamorphosis. ßFtz-F1 protein is necessary for transcriptional re-induction of Ecdysone early genes in response to the Ecdysone pulse that triggers the prepupal to pupal transition. We propose that ßFtz-F1 is also induced in the fat body and, in response to a second Ecdysone pulse, transcriptionally activates target genes responsible for fat-body dissociation. We have tested this model by recapitulating fat-body dissociation in fat body explants through the ectopic expression of ßFtz-F1 followed by incubation with Ecdysone.