The Drosophila ARC homolog regulates behavioral responses to starvation

Mattaliano, Mark D.; Montana, Enrico S.; Parisky, Katherine M.; Littleton, J Troy; Griffith, Leslie C.

doi:10.1016/j.mcn.2007.06.008

Cited by 67 publications

(101 citation statements)

References 52 publications

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“…A notable gene expression change shared by the Phax and Smn mutants was a fivefold increase in the Activity-regulated cytoskeleton associated protein 1 (Arc1) transcript (Supplemental Table S2). Arc1 functions in a well conserved hyperlocomotion response to starvation, and hence elevated levels in Phax and Smn mutants might be an indirect consequence of a disruption in nutrient acquisition in these animals (Mattaliano et al 2007). In summary, gene expression analysis uncovered a small number of overlapping changes that exceeded normal developmental fluctuations.…”

Section: Resultsmentioning

confidence: 99%

Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

Garcia

Wen

Praveen

et al. 2016

RNA

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Survival motor neuron (SMN) functions in the assembly of spliceosomal small nuclear ribonucleoproteins (snRNPs) that catalyze pre-mRNA splicing. Here, we used disruptions in Smn and two additional snRNP biogenesis genes, Phax and Ars2, to classify RNA processing differences as snRNP-dependent or gene-specific in Drosophila. Phax and Smn mutants exhibited comparable reductions in snRNAs, and comparison of their transcriptomes uncovered shared sets of RNA processing changes. In contrast, Ars2 mutants displayed only small decreases in snRNA levels, and RNA processing changes in these mutants were generally distinct from those identified in Phax and Smn animals. Instead, RNA processing changes in Ars2 mutants support the known interaction of Ars2 protein with the cap-binding complex, as splicing changes showed a clear bias toward the first intron. Bypassing disruptions in snRNP biogenesis, direct knockdown of spliceosomal proteins caused similar changes in the splicing of snRNP-dependent events. However, these snRNP-dependent events were largely unaltered in three Smn mutants expressing missense mutations that were originally identified in human spinal muscular atrophy (SMA) patients. Hence, findings here clarify the contributions of Phax, Smn, and Ars2 to snRNP biogenesis in Drosophila, and loss-of-function mutants for these proteins reveal differences that help disentangle cause and effect in SMA model flies.

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Section: Resultsmentioning

confidence: 99%

Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

Garcia

Wen

Praveen

et al. 2016

RNA

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“…In support of that notion, autophagy, which also facilitates increased cellular energy availability, has been shown to occur independently of AMPK activation (Williams et al 2009). Another candidate that may be involved in AMPK-independent regulation of AKH is the activity-regulated cytoskeletal-associated gene, which is specifically expressed in AKH cells; mutants in this gene fail to exhibit normal starvation-induced hyperactivity (Mattaliano et al 2007).…”

Section: Discussionmentioning

confidence: 99%

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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“…Since these insulin-like peptides have been shown to play a significant role in lifespan, in nutritional stress responses and in metabolic regulation (Baker and Thummel, 2007;Broughton et al, 2005;Giannakou and Partridge, 2007;Grönke et al, 2010;Rulifson et al, 2002;Tatar et al, 2001), the DTK signaling onto these cells may be of significance for the regulation of vital physiological functions. However, the IPCs are also known to regulate feeding behavior, locomotor activity, sleep-wakefulness and ethanol sensitivity, and they may do so independent of the insulin signaling pathway (Cognigni et al, 2011;Corl et al, 2005;Crocker et al, 2010;Mattaliano et al, 2007;Wu et al, 2005). Thus, activation or inhibition of signaling in the IPCs may result in actions that are…”

Section: Discussionmentioning

confidence: 99%

Regulation of insulin-producing cells in the adult Drosophila brain via the tachykinin peptide receptor DTKR

Birse

Söderberg

Luo

et al. 2011

Journal of Experimental Biology

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SUMMARYDrosophila insulin-like peptides (DILPs) play important hormonal roles in the regulation of metabolic carbohydrates and lipids, but also in reproduction, growth, stress resistance and aging. In spite of intense studies of insulin signaling in Drosophila the regulation of DILP production and release in adult fruit flies is poorly understood. Here we investigated the role of Drosophila tachykinin-related peptides (DTKs) and their receptors, DTKR and NKD, in the regulation of brain insulin-producing cells (IPCs) and aspects of DILP signaling. First, we show DTK-immunoreactive axon terminations close to the presumed dendrites of the IPCs, and DTKR immunolabeling in these cells. Second, we utilized targeted RNA interference to knock down expression of the DTK receptor, DTKR, in IPCs and monitored the effects on Dilp transcript levels in the brains of fed and starved flies. Dilp2 and Dilp3, but not Dilp5, transcripts were significantly affected by DTKR knockdown in IPCs, both in fed and starved flies. Both Dilp2 and Dilp3 transcripts increased in fed flies with DTKR diminished in IPCs whereas at starvation the Dilp3 transcript plummeted and Dilp2 increased. We also measured trehalose and lipid levels as well as survival in transgene flies at starvation. Knockdown of DTKR in IPCs leads to increased lifespan and a faster decrease of trehalose at starvation but has no significant effect on lipid levels. Finally, we targeted the IPCs with RNAi or ectopic expression of the other DTK receptor, NKD, but found no effect on survival at starvation. Our results suggest that DTK signaling, via DTKR, regulates the brain IPCs. Supplementary material available online at

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The Drosophila ARC homolog regulates behavioral responses to starvation

Cited by 67 publications

References 52 publications

Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

Transcriptomic comparison of Drosophila snRNP biogenesis mutants reveals mutant-specific changes in pre-mRNA processing: implications for spinal muscular atrophy

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

Regulation of insulin-producing cells in the adult Drosophila brain via the tachykinin peptide receptor DTKR

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