140584 - insulin like signalling.pdf (1.44 MB)
Insulin-like signalling influences the coordination of larval hemocyte number with body size in Drosophila melanogaster
journal contribution
posted on 2023-05-20, 17:16 authored by Bakopoulos, D, Forbes Beadle, L, Esposito, KM, Mirth, CK, Coral WarrCoral Warr, Johnson, TKBlood cells, known as hemocytes in invertebrates, play important and conserved roles in immunity, wound healing and tissue remodelling. The control of hemocyte number is therefore critical to ensure these functions are not compromised, and studies using Drosophila melanogaster are proving useful for understanding how this occurs. Recently, the embryonic patterning gene, torso-like (tsl), was identified as being required both for normal hemocyte development and for providing immunity against certain pathogens. Here, we report that Tsl is required specifically during the larval phase of hematopoiesis, and that tsl mutant larvae likely have reduced hemocyte numbers due to a reduced larval growth rate and compromised insulin signaling. Consistent with this, we find that impairing insulin-mediated growth, either by nutrient deprivation or genetically, results in fewer hemocytes. This is likely the result of impaired insulin-like signaling in the hemocytes themselves, since modulation of Insulin-like Receptor (InR) activity specifically in hemocytes causes concomitant changes to their population size in developing larvae. Taken together, our work reveals the strong relationship that exists between body size and hemocyte number, and suggests that insulin-like signaling contributes to, but is not solely responsible for, keeping these tightly aligned during larval development.
History
Publication title
G3: Genes, Genomes, GeneticsVolume
10Issue
7Pagination
2213-2220ISSN
2160-1836Department/School
Tasmanian School of MedicinePublisher
Genetics Society of AmericaPlace of publication
United StatesRights statement
Copyright © 2020 Bakopoulos et al. Licensed under Creative Commons Attribution 4.0 International (CC BY 4.0) https://creativecommons.org/licenses/by/4.0/Repository Status
- Open