Insect metamorphosis is regulated by the production, secretion and degradation of two peripheral hormones: 20-hydroxyecdysone (ecdysone) and juvenile hormone (JH). In addition to their roles in developmental regulation, increasing evidence suggests that these hormones are involved in innate immunity processes, such as phagocytosis and the induction of antimicrobial peptide (AMP) production. AMP regulation includes systemic responses and local responses, at surface epithelia that contact with the external environments. At pupariation, Drosophila melanogaster increases dramatically the expression of three AMP genes: drosomycin (drs), drosomycin-like 2 (drsl2) and drosomycin-like 5 (drsl5). Using D. melanogaster, we show that the expression of drs at pupariation is dependent on ecdysone signalling in the fat body. This systemic immune response involving drs expression in the fat body operates via the ecdysone downstream target, Broad-Z4. In parallel, ecdysone also regulates local responses, specifically through the activation of drsl2 expression in the gut. Finally, we establish the relevance of this ecdysone dependent AMP expression for the control of bacterial persistence by showing that flies lacking drs expression in the fat body have higher bacterial persistence over metamorphosis. Together, our data establishes a new role for ecdysone during pupariation. We propose that the co-option of immune mechanisms by the hormonal cascade responsible for controlling metamorphosis constitutes a pre-emptive mechanism to control bacterial numbers in the pupa and increase developmental success.
Hormonal regulations in insect metamorphosis: A review
