Fat body secreted SPARC promotes Ilp2 release and systemic growth in Drosophila larvae
Abstract
Background: The growth of Drosophila larvae is strongly influenced by the available food. Depending on the quality and quantity of ingested nutrients, the larval fat body secretes systemic signals that control the growth of other organs. The identity of these signals is not fully understood yet.
Results: We describe a reporter-based in vivo screen that allowed the systematic gene knockdown in the signal-producing fat body and simultaneously measured the resulting growth effects in the signal-receiving larval peripheral tissues. This screen led to the identification of the matricellular protein SPARC/BM-40 (Secreted protein acidic and rich in cysteine/Basement-membrane protein 40) as a novel factor controlling the release of insulin from neurosecretory cells and thereby controlling systemic animal growth. Synthetic human SPARC can substitute for Drosophila SPARC, revealing a novel evolutionarily conserved signaling axis.
Conclusions: The evolutionarily conserved protein SPARC is identified as a novel incretin-like signal that can promote the endocrine release of insulin in vivo.
Related
- The Histone Methyltransferase KMT2D promotes Natural Killer cell effector molecule release
- The NimB2 opsonin promotes S. aureus recognition by macrophages in Drosophila melanogaster
- AMPK-dependent brain-wide norepinephrine release promotes recovery from metabolic coma in mice
- The actin-binding protein drebrin interacts with the respiratory syncytial virus matrix protein and promotes virus particle release.
- Engineered living materials suppress uropathogenic E. coli growth and invasion of urothelial cells through sustained probiotic release
BibTeX
@article{carreno2026body,
title = {{Fat body secreted SPARC promotes Ilp2 release and systemic growth in Drosophila larvae}},
author = {Oriel Carreno and Maria Gallant and Katharina Grund-Müller and Sander Liessem and Gertrud Gramlich and Maria Piera Trilla and Apoorva Baluapuri and Yalda Ghoreishi and Jennifer Gerlach and Jan M. Ache and Christian Wegener and Peter Gallant},
journal = {BMC Biology},
year = {2026},
month = oct,
doi = {10.1186/s12915-026-02761-x},
url = {https://link.springer.com/10.1186/s12915-026-02761-x},
note = {CC BY 4.0},
}
RIS
TY - JOUR
TI - Fat body secreted SPARC promotes Ilp2 release and systemic growth in Drosophila larvae
AU - Oriel Carreno
AU - Maria Gallant
AU - Katharina Grund-Müller
AU - Sander Liessem
AU - Gertrud Gramlich
AU - Maria Piera Trilla
AU - Apoorva Baluapuri
AU - Yalda Ghoreishi
AU - Jennifer Gerlach
AU - Jan M. Ache
AU - Christian Wegener
AU - Peter Gallant
PY - 2026
DA - 2026/10/13
JO - BMC Biology
DO - 10.1186/s12915-026-02761-x
UR - https://link.springer.com/10.1186/s12915-026-02761-x
AB - Background: The growth of Drosophila larvae is strongly influenced by the available food. Depending on the quality and quantity of ingested nutrients, the larval fat body secretes systemic signals that control the growth of other organs. The identity of these signals is not fully understood yet. Results: We describe a reporter-based in vivo screen that allowed the systematic gene knockdown in the signal-producing fat body and simultaneously measured the resulting growth effects in the signal-receiving larval peripheral tissues. This screen led to the identification of the matricellular protein SPARC/BM-40 (Secreted protein acidic and rich in cysteine/Basement-membrane protein 40) as a novel factor controlling the release of insulin from neurosecretory cells and thereby controlling systemic animal growth. Synthetic human SPARC can substitute for Drosophila SPARC, revealing a novel evolutionarily conserved signaling axis. Conclusions: The evolutionarily conserved protein SPARC is identified as a novel incretin-like signal that can promote the endocrine release of insulin in vivo.
SN - 1741-7007
ER -