ESPE Yearbook of Paediatric Endocrinology

To read the full abstract: Curr Biol 2019;29:813–822 e4.

In vertebrates, puberty is the critical transitional step which leads to major somatic changes and the acquisition of the reproduction function. At the molecular level, puberty equates to the reactivation of the gonadotropic axis after a period of childhood quiescence, and hence increases sex steroid production. This reactivation is controlled by many neuropeptides and neurotransmitters, with kisspeptin as a major actor. In Drosophila, the transition from juvenile to adult corresponds to the metamorphosis, which is marked by an increase in ecdysone secretion by the prothoracic gland under the control of the prothoracicotropic hormone (PTTH). This pathway strongly contributes to the juvenile-maturation transition (JMT).

Here, the authors described AstA as a neuropeptide which acts in the fruit fly through a specific receptor (AstAR1) expressed in PTTH producing neurons. AstAR1 controls PTTH secretion and thereby regulates the JMT. Interestingly, AstA is also expressed in brain insulin-producing cells (IPCs) to promote insulin secretion and systemic growth. AstA/AstAR1 signaling is maximal prior to maturation, indicating a specific activation of this pathway at this developmental stage.

Interestingly, AstA and AstAR1 are homologous to Kiss1 and Kiss1R, respectively and many biological features reported for AstA and AstAR1 here in the fruit fly (increased activity at the end of the juvenile period, expression in insulin secreting cells, control of sexual hormone synthesis and secretion) have also been described for Kiss1 and Kiss1R in mammals. This work therefore demonstrates that JMT and puberty are under a similar ancestral mechanism, which relatively well conserved during evolution. Similar questions remain for both JMT and puberty. Which signal triggers the increase in AstA/AstAR1 or Kiss1/Kiss1R signaling at the end of the juvenile period?