AKH Signaling in D. melanogaster Alters Larval Development in a Nutrient-Dependent Manner That Influences Adult Metabolism

Bryon N. Hughson, Mary Jane Shimell, Michael B. O’Connor

Research output: Contribution to journalArticlepeer-review

9 Scopus citations


Metabolism, growth, and development are intrinsically linked, and their coordination is dependent upon inter-organ communication mediated by anabolic, catabolic, and steroid hormones. In Drosophila melanogaster, the corpora cardiaca (CC) influences metabolic homeostasis through adipokinetic hormone (AKH) signaling. AKH has glucagon-like properties and is evolutionarily conserved in mammals as the gonadotropin-releasing hormone, but its role in insect development is unknown. Here we report that AKH signaling alters larval development in a nutrient stress-dependent manner. This activity is regulated by the locus dg2, which encodes a cGMP-dependent protein kinase (PKG). CC-specific downregulation of dg2 expression delayed the developmental transition from larval to pupal life, and altered adult metabolism and behavior. These developmental effects were AKH-dependent, and were observed only in flies that experienced low nutrient stress during larval development. Calcium-mediated vesicle exocytosis regulates ecdysteroid secretion from the prothoracic gland (PG), and we found that AKH signaling increased cytosolic free calcium levels in the PG. We identified a novel pathway through which PKG acts in the CC to communicate metabolic information to the PG via AKH signaling. AKH signaling provides a means whereby larval nutrient stress can alter developmental trajectories into adulthood.

Original languageEnglish (US)
Article number619219
JournalFrontiers in Physiology
StatePublished - Feb 23 2021

Bibliographical note

Funding Information:
We thank Professor J. Dason for assistance with the conception, troubleshooting, design, and analysis of calcium imaging experiments, Anders Vesterberg for wing size and cell quantification. We thank all three reviewers for their insightful and productive input. Funding. BNH was supported by a Natural Science and Engineering Council of Canada and Canadian Institute for Advanced Research grant (to Marla B. Sokolowski), and MS and MBO were supported by the NIH grant R35GM-118029.

Publisher Copyright:
© Copyright © 2021 Hughson, Shimell and O’Connor.


  • AKH
  • PKG
  • adipokinetic hormone
  • corpora cardiaca
  • development
  • dg2
  • metabolism
  • prothoracic gland

PubMed: MeSH publication types

  • Journal Article


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