Factors that regulate insulin producing cells and their output in Drosophila.
271
TL;DR: This review summarizes what is known about regulation of production and release of ILPs in Drosophila with focus on insulin signaling in the daily life of the fly and physiological conditions under which IPC activity may be regulated, including nutritional states, stress and diapause induction.
read more
Abstract: Insulin-like peptides (ILPs) and growth factors (IGFs) not only regulate development, growth, reproduction, metabolism, stress resistance, and lifespan, but also certain behaviors and cognitive functions. ILPs, IGFs, their tyrosine kinase receptors and downstream signaling components have been largely conserved over animal evolution. Eight ILPs have been identified in Drosophila (DILP1-8) and they display cell and stage-specific expression patterns. Only one insulin receptor, dInR, is known in Drosophila and most other invertebrates. Nevertheless, the different DILPs are independently regulated transcriptionally and appear to have distinct functions, although some functional redundancy has been revealed. This review summarizes what is known about regulation of production and release of DILPs in Drosophila with focus on insulin signaling in the daily life of the fly. Under what conditions are DILP-producing cells (IPCs) activated and which factors have been identified in control of IPC activity in larvae and adult flies? The brain IPCs that produce DILP2, 3 and 5 are indirectly targeted by DILP6 and a leptin-like factor from the fat body, as well as directly by a few neurotransmitters and neuropeptides. Serotonin, octopamine, GABA, short neuropeptide F (sNPF), corazonin and tachykinin-related peptide have been identified in Drosophila as regulators of IPCs. The GABAergic cells that inhibit IPCs and DILP release are in turn targeted by a leptin-like peptide (unpaired 2) from the fat body, and the IPC-stimulating corazonin/sNPF neurons may be targeted by gut-derived peptides. We also discuss physiological conditions under which IPC activity may be regulated, including nutritional states, stress and diapause induction.
read more
Chat with Paper
AI Agents for this Paper
Find similar papers on Google Scholar, PubMed and Arxiv
Write a critical review of this paper
Analyze citations of this paper to find unaddressed research gaps
Citations
Thermosensation and Temperature Preference: From Molecules to Neuronal Circuits in Drosophila
Meng-Hsuan Chiang,Yu-Chun Lin +1 more
TL;DR: This review provides a comprehensive overview of the current understanding of thermosensation and temperature preference in Drosophila, and encompasses various aspects, such as the mechanisms by which flies sense temperature, the effects of internal and external factors on temperature preference, and the adaptive strategies employed by flies in extreme-temperature environments.
2
Wider Implications
Rose Evison,Jeremy Dawson +1 more
- 03 Feb 2022
TL;DR: A wide range of chemical and physical manipulators of diapause are known, many of which are species-specific as discussed by the authors , and they have utility for managing domesticated species, for mass rearing of insects for sterile release, and for stockpiling valuable genetic lines or parasitoids used in the biological control industry.
2
Drosophila melanogaster as a model organism for diabetes II treatment by the ethyl acetate fraction of Atriplex halimus L.
TL;DR: The results indicated the therapeutic activity of the A. halimus ethyl acetate fraction against induced T2D in Drosophila larvae, which may be attributed to flavonoids, which are the main components of the A. halimus ethyl acetate fraction.
2
Linking Nutrients to Growth through a Positive Feedback Loop.
TL;DR: In this issue of Developmental Cell, Okamoto and Nishimura (2015) identify a positive feedback loop between neuronal cells that maintains insulin signaling and growth under restricted nutritional conditions.
2
Cell Death Pathways in an Unconventional Invertebrate Model
Enzo Ottaviani,Davide Malagoli +1 more
- 01 Jan 2016
TL;DR: The prodeath effects and the pathways activated by the mitochondria-targeting drugs 2-deoxy- d -ribose, sodium nitroprusside, or oligomycin A in the IPLB-LdFB cell line derived from the unconventional insect model Lymantria dispar are described.
2
References
Algebraic correction methods for computational assessment of clone overlaps in DNA fingerprint mapping.
TL;DR: A straightforward algebraic correction procedure is proposed, which takes the Sulston score as a provisional value and applies a power-law equation to obtain an improved result, which provides a vastly improved probabilistic description of hypothesized clone overlaps.
A mutant Drosophila insulin receptor homolog that extends life-span and impairs neuroendocrine function.
TL;DR: It is concluded that juvenile hormone deficiency, which results from InR signal pathway mutation, is sufficient to extend life-span, and that in flies, insulin-like ligands nonautonomously mediate aging through retardation of growth or activation of specific endocrine tissue.
1.6K
Using FlyAtlas to identify better Drosophila melanogaster models of human disease
TL;DR: FlyAtlas provides the most comprehensive view yet of expression in multiple tissues of Drosophila melanogaster, demonstrating the limitations of whole-organism approaches to functional genomics and allowing modeling of a simple tissue fractionation procedure that should improve detection of weak or tissue-specific signals.
1.6K
Extension of Life-Span by Loss of CHICO, a Drosophila Insulin Receptor Substrate Protein
David J. Clancy,David Gems,Lawrence G. Harshman,Sean Oldham,Hugo Stocker,Ernst Hafen,Sally J. Leevers,Linda Partridge +7 more
TL;DR: It is found that mutation of chico extends fruit fly median life-span by up to 48% in homozygotes and 36% in heterozygotes, and the role of insulin/IGF signaling in regulating animal aging is evolutionarily conserved.
The plasticity of aging: insights from long-lived mutants.
TL;DR: Mutations in genes affecting endocrine signaling, stress responses, metabolism, and telomeres can all increase the life spans of model organisms, leading to a mechanistic understanding of how these two processes--aging and disease susceptibility--are linked.
1.4K