ßFTZ-F1 and Matrix metalloproteinase 2 are required for fat-body remodeling in Drosophila

During metamorphosis, holometabolous insects eliminate obsolete larval tissues via programmed cell death. In contrast, tissues required for further development are retained and often remodeled to meet the needs of the adult fly. The larval fat body is involved in fueling metamorphosis, and thus it escapes cell death and is instead remodeled during prepupal development. The molecular mechanisms by which the fat body escapes programmed cell death have not yet been described, but it has been established that fat-body remodeling requires 20-hydroxyecdysone (20E) signaling. We have determined that 20E signaling is required within the fat body for the cell-shape changes and cell detachment that are characteristic of fat-body remodeling. We demonstrate that the nuclear hormone receptor ßFTZ-F1 is a key modulator of 20E hormonal induction of fat body remodeling and Matrix metalloproteinase 2 (MMP2) expression in the fat body. We show that induction of MMP2 expression in the fat body requires 20E signaling, and that MMP2 is necessary and sufficient to induce fat-body remodeling.

► Fat-body remodeling requires 20E signaling and the competence factor ßFTZ-F1.
► MMP2 is necessary and sufficient to promote fat-body remodeling.
► ßFTZ-F1 and 20E signaling function in inducing MMP2 expression in fat body.
► Fat-body remodeling is a tissue autonomous process.