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
The Diapause State
03 Feb 2022
TL;DR: In diapause, development is halted or dramatically retarded, the cell cycle is arrested, metabolic rates are suppressed, and a global metabolic shift from aerobic to anaerobic metabolism is evident as discussed by the authors .
1
Nutritional state-dependent modulation of Insulin-Producing Cells in Drosophila
Rituja S. Bisen,Fathima Mukthar Iqbal,Federico Cascino-Milani,Till Bockemühl,Jan M. Ache +4 more
- 02 Jul 2024
TL;DR: This study investigates the modulation of Insulin-Producing Cells (IPCs) in Drosophila by nutritional state, revealing IPC activity is strongly influenced by hemolymph sugar levels and regulated by parallel glucose-sensing neurons to maintain metabolic homeostasis.
1
Cloning of the Bombyx mori short neuropeptide F receptor (BsNPF-R) cDNA
Hyojung Shin,Kisang Kwon,Sun Mee Hong,Hong Geun Kim,Kwan-Ho Park,Ji-Young Choi,Seung Whan Kim,Kweon Yu,O-Yu Kwon +8 more
TL;DR: The synthesized sNPF of a silkworm regulated the BsNPF-R mRNA expression through the cell-based functional analysis, showing that a strong expression was detected at the midgut, post-silk gland, Malpighian, and testis; however, a weak expression was at the fat body, hemocyte, and ovary.
1
Morphological and functional effects of insulin signaling and the bHLH transcription factor Dimmed on different neuron types in Drosophila
Yiting Liu
- 01 Jan 2016
TL;DR: In Drosophila, the insulin signaling pathway is at the interface between dietary conditions and control of growth and development, reproduction, stress responses and life span.
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