Abstract
SUMOylation participates in ecdysteroid biosynthesis at the onset of metamorphosis in Drosophila melanogaster. Silencing the Drosophila SUMO homologue smt3 in the prothoracic gland leads to reduced lipid content, low ecdysone titers, and a block in the larval–pupal transition. Here we show that the SR-BI family of Scavenger Receptors mediates SUMO functions. Reduced levels of Snmp1 compromise lipid uptake in the prothoracic gland. In addition, overexpression of Snmp1 is able to recover lipid droplet levels in the smt3 knockdown prothoracic gland cells. Snmp1 expression depends on Ftz-f1 (an NR5A-type orphan nuclear receptor), the expression of which, in turn, depends on SUMO. Furthermore, we show by in vitro and in vivo experiments that Ftz-f1 is SUMOylated. RNAi–mediated knockdown of ftz-f1 phenocopies that of smt3 at the larval to pupal transition, thus Ftz-f1 is an interesting candidate to mediate some of the functions of SUMO at the onset of metamorphosis. Additionally, we demonstrate that the role of SUMOylation, Ftz-f1, and the Scavenger Receptors in lipid capture and mobilization is conserved in other steroidogenic tissues such as the follicle cells of the ovary. smt3 knockdown, as well as ftz-f1 or Scavenger knockdown, depleted the lipid content of the follicle cells, which could be rescued by Snmp1 overexpression. Therefore, our data provide new insights into the regulation of metamorphosis via lipid homeostasis, showing that Drosophila Smt3, Ftz-f1, and SR-BIs are part of a general mechanism for uptake of lipids such as cholesterol, required during development in steroidogenic tissues.
Highlights
Larval molting and metamorphosis in Drosophila melanogaster relies on pulses of ecdysteroid hormones
Reduced levels of the small ubiquitin-like modifier SUMO in the prothoracic gland block the synthesis of ecdysone, as SUMO is needed for cholesterol intake
The expression of the Scavenger Receptors depends on Ftzf1, a nuclear transcription factor homologous to mammalian Steroidogenic factor 1 (SF-1)
Summary
Larval molting and metamorphosis in Drosophila melanogaster relies on pulses of ecdysteroid hormones. The prothoracic gland (PG) is the tissue responsible for the synthesis of the steroid hormone ecdysone that is secreted to the hemolymph and converted to 20-hydroxyecdysone (20E) in target tissues [1]. Cholesterol is the precursor of all steroid hormones. Cholesterol is converted to 20E through a series of enzymatic reactions that involve the cytochrome P450 enzymes coded by the Halloween genes spook, spookier, phantom (phm), disembodied (dib), shadow, shade and the Rieske non-heme iron oxigenase gene neverland [2,3]. A similar transcriptional cascade is required during embryogenesis and could be required for each larval molting [5]. Many of the aspects involved in the regulation of ecdysteroid biosynthesis remain unknown
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