scholarly journals Nutrient Availability and Growth: Regulation of Insulin Signaling by dFOXO/FOXO1

Cell Cycle ◽  
2006 ◽  
Vol 5 (5) ◽  
pp. 503-505 ◽  
Author(s):  
Oscar Puig ◽  
Robert Tjian
Genetics ◽  
2021 ◽  
Author(s):  
Himani Pathak ◽  
Ananthakrishnan Vijaykumar Maya ◽  
Abdul Basith Tanari ◽  
Sohela Sarkar ◽  
Jishy Varghese

AbstractInsulin signaling in Drosophila has a significant role in regulating growth, metabolism, fecundity, stress response, and longevity. The molecular mechanism by which insulin signaling regulates these vital processes is dependent on the nutrient status and oxygen availability of the organism. In a genetic screen to identify novel genes that regulate Drosophila insulin signaling, we discovered lumens interrupted (lint), a gene that has previously been shown to act in tracheal development. The knockdown of lint gene expression using a Dilp2Gal4 driver which expresses in the neuronal insulin producing cells (IPCs), led to defects in systemic insulin signaling, metabolic status and growth. However, our analysis of lint knockdown phenotypes revealed that downregulation of lint in the trachea and not IPCs was responsible for the growth phenotypes, as the Gal4 driver is also expressed in the tracheal system. We found various tracheal terminal branch defects, including reduction in the length as well as number of branches in the lint knockdown background. Our study reveals that substantial effects of lint downregulation arose because of tracheal defects, which induced tissue hypoxia, altered systemic insulin/TOR signaling, and resulted in effects on developmental growth regulation.


2013 ◽  
Vol 8 (1) ◽  
pp. 65-78 ◽  
Author(s):  
Peter W. Bates ◽  
◽  
Yu Liang ◽  
Alexander W. Shingleton ◽  

2021 ◽  
Author(s):  
Shrivani Sriskanthadevan-Pirahas ◽  
Michael J Turingan ◽  
Joel S Chahal ◽  
Erin Thorson ◽  
Savraj Grewal

Animals need to adapt their growth to fluctuations in nutrient availability to ensure proper development and survival. These adaptations often rely on specific nutrient-sensing tissues and their control of whole-body physiology through inter-organ communication. While the signaling mechanisms that underlie this communication are well studied, the contributions of metabolic alterations in the nutrient-sensing tissues are less clear. Here, we show how reprogramming of adipose mitochondrial metabolism controls whole-body growth in Drosophila larvae. We find that dietary nutrients alter fat body mitochondrial morphology to lower their bioenergetic activity, which we see can rewire fat body glucose metabolism. Strikingly, we find that genetic reduction of mitochondrial bioenergetics just in the fat body is sufficient to accelerate body growth and development. These growth effects are caused by inhibition of the fat-derived adipokine, TNFα/Eiger, which leads to enhanced systemic insulin signaling, the main hormonal stimulator of body growth. Our work reveals how reprogramming of mitochondrial metabolism in one nutrient-sensing tissue is able to couple whole body growth to nutrient availability.


2008 ◽  
Vol 8 (1) ◽  
pp. 65-76 ◽  
Author(s):  
Xiaocheng C. Dong ◽  
Kyle D. Copps ◽  
Shaodong Guo ◽  
Yedan Li ◽  
Ramya Kollipara ◽  
...  

2008 ◽  
Vol 180 (4) ◽  
pp. 691-696 ◽  
Author(s):  
Kieran F. Harvey ◽  
Jaakko Mattila ◽  
Avi Sofer ◽  
F. Christian Bennett ◽  
Matthew R. Ramsey ◽  
...  

FOXO is thought to function as a repressor of growth that is, in turn, inhibited by insulin signaling. However, inactivating mutations in Drosophila melanogaster FOXO result in viable flies of normal size, which raises a question over the involvement of FOXO in growth regulation. Previously, a growth-suppressive role for FOXO under conditions of increased target of rapamycin (TOR) pathway activity was described. Here, we further characterize this phenomenon. We show that tuberous sclerosis complex 1 mutations cause increased FOXO levels, resulting in elevated expression of FOXO-regulated genes, some of which are known to antagonize growth-promoting pathways. Analogous transcriptional changes are observed in mammalian cells, which implies that FOXO attenuates TOR-driven growth in diverse species.


Cell ◽  
2016 ◽  
Vol 166 (4) ◽  
pp. 867-880 ◽  
Author(s):  
Cristina García-Cáceres ◽  
Carmelo Quarta ◽  
Luis Varela ◽  
Yuanqing Gao ◽  
Tim Gruber ◽  
...  

Author(s):  
О.Л. Жданова ◽  
O.L. Zhdanova

In the paper set of models that take into account various mechanisms for ectokrine regulation of phytoplankton growth are proposed and studied. The considered models are following: with a nonlinear dependence of phytoplankton growth rate on the concentration of the metabolite in the environment; with a metabolite, which increases both the growth rate and mortality of the phytoplankton; with two different metabolites, one of which increases the rate of growth of phytoplankton, and the second - is reduced. These models are modifications of the classical space-time model of the dynamics of phytoplankton, linking change in its density and the concentration of nutrients in space and time, which do not consider the mechanism of ectokrine growth regulation. By the means of the model it has been shown, that the metabolites secreted by algae are able to stabilize the growth of phytoplankton in conditions of excessive nutrient availability.


2017 ◽  
Author(s):  
Kurt Buhler ◽  
Jason Clements ◽  
Mattias Winant ◽  
Veerle Vulsteke ◽  
Patrick Callaerts

AbstractGrowth and maturation are coordinated processes in all animals. Integration of internal cues, such as signalling pathways, with external cues such as nutritional status is paramount for an orderly progression of development in function of growth. In Drosophila, this coordination involves insulin and steroid signalling, but the mechanisms by which this occurs and how they are coordinated are incompletely understood. We show that production of the bioactive 20-hydroxyecdysone by the enzyme Shade in the fat body is a nutrient-dependent process. We demonstrate that during fed conditions, Shade plays a role in growth regulation, as knockdown of shade in the fat body resulted in growth defects and perturbed expression and release of the Drosophila insulin-like peptides from the insulin-producing cells (IPCs). We identify the trachea and IPCs as direct targets through which 20-hydroxyecdysone regulates insulin-signaling. The identification of the trachea-dependent regulation of insulin-signaling exposes an important variable that may have been overlooked in other studies focusing on insulin-signaling in Drosophila. Finally, we show with IPC-specific manipulations that 20E may both be a growth-promoting and growth-inhibiting signal in the IPCs acting through different nuclear receptors. Our findings provide a potentially conserved, novel mechanism by which nutrition can modulate steroid hormone bioactivation, reveal an important caveat of a commonly used transgenic tool to study IPC function and yield further insights as to how steroid and insulin signalling are coordinated during development to regulate growth and developmental timing.


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