Characteristics of genes up-regulated and down-regulated after 24 h starvation in the head of Drosophila

Fujikawa, Keiko; Takahashi, Aya; Nishimura, Azusa; Itoh, Masanobu; Takano-Shimizu, Toshiyuki; Ozaki, Mamiko

doi:10.1016/j.gene.2009.06.017

Cited by 51 publications

(55 citation statements)

References 41 publications

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“…We found that the AKH expression profile was similarly independent of genotype as it pertained to AMPK function and expression ( Figure 2C). We did find a significant downregulation of AKH expression due to starvation, which is supported by previous experiments showing downregulation of aspects of the AKH-signaling pathway, specifically the AKH receptor (Fujikawa et al 2009) and other downstream effectors of AKH, including the TAG lipase and other metabolic enzymes (Grönke et al 2005).…”

Section: Reduced Ampk Function Affects Neither Akh Cell Survival Nor supporting

confidence: 90%

Energy-Dependent Modulation of Glucagon-Like Signaling inDrosophilavia the AMP-Activated Protein Kinase

Braco¹,

Gillespie²,

Alberto³

et al. 2012

Genetics

102

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Adipokinetic hormone (AKH) is the equivalent of mammalian glucagon, as it is the primary insect hormone that causes energy mobilization. In Drosophila, current knowledge of the mechanisms regulating AKH signaling is limited. Here, we report that AMP-activated protein kinase (AMPK) is critical for normal AKH secretion during periods of metabolic challenges. Reduction of AMPK in AKH cells causes a suite of behavioral and physiological phenotypes resembling AKH cell ablations. Specifically, reduced AMPK function increases life span during starvation and delays starvation-induced hyperactivity. Neither AKH cell survival nor gene expression is significantly impacted by reduced AMPK function. AKH immunolabeling was significantly higher in animals with reduced AMPK function; this result is paralleled by genetic inhibition of synaptic release, suggesting that AMPK promotes AKH secretion. We observed reduced secretion in AKH cells bearing AMPK mutations employing a specific secretion reporter, confirming that AMPK functions in AKH secretion. Live-cell imaging of wild-type AKH neuroendocrine cells shows heightened excitability under reduced sugar levels, and this response was delayed and reduced in AMPK-deficient backgrounds. Furthermore, AMPK activation in AKH cells increases intracellular calcium levels in constant high sugar levels, suggesting that the underlying mechanism of AMPK action is modification of ionic currents. These results demonstrate that AMPK signaling is a critical feature that regulates AKH secretion, and, ultimately, metabolic homeostasis. The significance of these findings is that AMPK is important in the regulation of glucagon signaling, suggesting that the organization of metabolic networks is highly conserved and that AMPK plays a prominent role in these networks.

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Section: Reduced Ampk Function Affects Neither Akh Cell Survival Nor supporting

confidence: 90%

Energy-Dependent Modulation of Glucagon-Like Signaling inDrosophilavia the AMP-Activated Protein Kinase

Braco¹,

Gillespie²,

Alberto³

et al. 2012

Genetics

102

View full text Add to dashboard Cite

show abstract

“…Fujikawa et al examined the gene expression changes in flies starved for 24 hours and observed 65 genes whose expression increased under starvation, and 48 genes whose expression decreased [27]. In both our chronic DR and Fujikawa et al experiments the number of up-regulated genes exceeded the number of down-regulated genes although in slightly greater proportion in chronic DR (172% in DR versus 135% in starvation).…”

Section: Resultsmentioning

confidence: 61%

Dietary switch reveals fast coordinated gene expression changes in Drosophila melanogaster

Whitaker

Gil

Ding

et al. 2014

Aging

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Dietary restriction (DR) reduces age-specific mortality and increases lifespan in many organisms. DR elicits a large number of physiological changes, however many are undoubtedly not related to longevity. Whole-genome gene expression studies have typically revealed hundreds to thousands of differentially expressed genes in response to DR, and a key open question is which subset of genes mediates longevity. Here we performed transcriptional profiling of fruit flies in a closely spaced time series immediately following a switch to the DR regime and identified four patterns of transcriptional dynamics. Most informatively we find 144 genes rapidly switched to the same level observed in the DR cohort and are hence strong candidates as proximal mediators of reduced mortality upon DR. This class was enriched for genes involved in carbohydrate and fatty acid metabolism. Folate biosynthesis was the only pathway enriched for gene up-regulated upon DR. Four among the down-regulated genes are involved in key regulatory steps within the pentose phosphate pathway, which has been previously associated with lifespan extension in Drosophila. Combined analysis of dietary switch with whole-genome time-course profiling can identify transcriptional responses that are closely associated with and perhaps causal to longevity assurance conferred by dietary restriction.

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“…(32). Previous studies have explored the transcriptional response to starvation in whole body samples of third instar larvae (33) or adult flies (34), as well as in isolated heads (35). These studies provided a general view of the transcriptional response to starvation, yet the fasting response of specific tissues has not been comprehensively compared to date.…”

Section: Resultsmentioning

confidence: 99%

Control of metabolic adaptation to fasting by dILP6-induced insulin signaling in Drosophila oenocytes

Chatterjee

Katewa

et al. 2014

Proc. Natl. Acad. Sci. U.S.A.

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Metabolic adaptation to changing dietary conditions is critical to maintain homeostasis of the internal milieu. In metazoans, this adaptation is achieved by a combination of tissue-autonomous metabolic adjustments and endocrine signals that coordinate the mobilization, turnover, and storage of nutrients across tissues. To understand metabolic adaptation comprehensively, detailed insight into these tissue interactions is necessary. Here we characterize the tissue-specific response to fasting in adult flies and identify an endocrine interaction between the fat body and liverlike oenocytes that regulates the mobilization of lipid stores. Using tissue-specific expression profiling, we confirm that oenocytes in adult flies play a central role in the metabolic adaptation to fasting. Furthermore, we find that fat body-derived Drosophila insulinlike peptide 6 (dILP6) induces lipid uptake in oenocytes, promoting lipid turnover during fasting and increasing starvation tolerance of the animal. Selective activation of insulin/IGF signaling in oenocytes by a fat body-derived peptide represents a previously unidentified regulatory principle in the control of metabolic adaptation and starvation tolerance.T o maintain metabolic homeostasis during fasting periods, metazoans have to coordinate the mobilization of glycogen, lipids, and protein, ensuring an adequate energy supply across tissues. In addition to tissue-autonomous metabolic adjustments, endocrine signals are therefore critical components of the fasting response (1, 2). In mammals, the liver is central to adjusting intermediary metabolism during fasting. Starvation stimulates lipid accumulation in hepatocytes, which oxidize these lipids to provide energy in the form of ketone bodies for other tissues. Hepatocytes also respond to glucagon and insulin signals to control the expression of enzymes involved in glycogenolysis and gluconeogenesis, lipolysis, fatty acid oxidation, and ketogenesis, all regulated by a battery of transcription factors that include forkhead box O (Foxo), cAMP-response element binding (CREB), peroxisome proliferator-activated receptor gamma, coactivator 1 alpha (PGC1a), and hepatocyte nuclear factor 4a (HNF4a) (3-5). At the same time, the liver integrates a suite of endocrine signals derived from major energy storing and consuming tissues, such as the brain, the adipose tissue, and the muscle (1). Deregulation of these processes can lead to hepatic steatosis and is a major cause of metabolic diseases, including diabetes and metabolic syndrome (1,3,6).Drosophila has emerged as a productive model organism in which to characterize the endocrine regulation of metabolic adaptation (7,8). The central function of the liver in metabolic adaptation of flies is shared by the fat body and oenocytes. Whereas the fat body is an important glycogen and fat storage organ in flies, it also serves as an endocrine organ to coordinate metabolic homeostasis (9-12). Oenocytes have a critical role in lipid mobilization and turnover in larvae, accumulating lipids during s...

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Characteristics of genes up-regulated and down-regulated after 24 h starvation in the head of Drosophila

Cited by 51 publications

References 41 publications

Energy-Dependent Modulation of Glucagon-Like Signaling inDrosophilavia the AMP-Activated Protein Kinase

Energy-Dependent Modulation of Glucagon-Like Signaling inDrosophilavia the AMP-Activated Protein Kinase

Dietary switch reveals fast coordinated gene expression changes in Drosophila melanogaster

Control of metabolic adaptation to fasting by dILP6-induced insulin signaling in Drosophila oenocytes

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