AKH-FOXO pathway regulates starvation-induced sleep loss through remodeling of the small ventral lateral neuron dorsal projections

He, Qiankun; Du, Juan; Wei, Liya; Zhao, Zhangwu

doi:10.1371/journal.pgen.1009181

Cited by 23 publications

(18 citation statements)

References 40 publications

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“…A time-restriced increased feeding in AKH-deficient flies is also suggested by the transcriptional up-regulation of the orexigenic peptides NPF and CCHa2 in AKH mutant flies, which paradoxically was not found to be coupled to increased total feeding [71]. Wildtype flies increase Akh mRNA levels 3h after the dark-light or light-dark transition, the time points at which starved flies showed pronounced starvation-induced hyperactivity [68]. Interestingly, times of increased sucrose feeding in flies with ablated APCs occurred around ZT3 (significant increase, coupled with low glucose titres) and ZT15 (small and insignificant increase, coupled with high glucose titres) in our study.…”

Section: Discussionmentioning

confidence: 95%

Endocrine fine-tuning of daily locomotor activity patterns under non-starving conditions in Drosophila

Pauls

Selcho

Raederscheidt

et al. 2020

Preprint

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body ATP-sensitive potassium channels [6]. This triggers AKH release in a calcium-and AMP-activated protein kinase-dependent fashion [13]. Similar to glucagon, AKH acts on energy stores in the fat body by mobilising carbohydrates in form of the haemolymph sugar trehalose (hypertrehalosaemic effect), and by mobilising lipid depots (adipokinetic effect) [8,[14][15][16].OA, an analogue to vertebrate noradrenaline, is considered to act as an insect stress or arousal hormone [17]. OA is produced by octopaminergic neurons (OANs) located mostly along the midline in the brain and ventral nerve cord [18]. Among other functions, OA exerts myotropic effects on skeletal muscles [19] and mediates the adaptation of muscle metabolism to the physiological demands of locomotion [20][21][22].Both AKH and OA are crucial for starvation-induced hyperactivity, as this behaviour is absent in flies with impaired AKH or OA signalling [4,5,[7][8][9]. AKH activates a subset of OANs which are required for starvation-induced hyperactivity [5,9]. These neurons express receptors for AKH and Drosophila insulin-like peptides (DILPs). DILPs act antagonistically to AKH, and suppress starvation-induced hyperactivity via the OANs [9]. Yu and colleagues (2016) showed that the AKH-dependent increase in locomotor activity upon starvation represents a neuromodulatory and behavioural role of AKH and is not an indirect consequence of altered energy metabolism.Remarkably, studies in various insect species suggest that AKH and also OA play a role in the regulation of locomotor activity when the insects have free access to food (reviewed in [23]). For example, the circulating haemolymph titres of AKH correlate positively with daily rhythms in walking activity in the linden bug Pyrrhocoris apterus [24,25]. In Pyrrhocoris [26,27], crickets [28] and the cockroach Periplaneta americana [29,30], injection into the haemolymph or topical application of AKH induces a strong increase in locomotor activity in ad libitum fed animals, independent of the time of day [27,29]. Also in Drosophila, genetic overexpression of AKH enhances locomotor activity when food is freely available [31]. Unlike for starvation-induced hyperactivity, however, it is unclear whether and how AKH:OAN signalling contributes to shape daily activity under ad libitum feeding conditions, or whether increased AKH signalling is a consequence of a locomotor-induced increase in energy demands. Cockroach AKHs are known to increase the spontaneous neuronal activity of octopaminergic dorsal unpaired median neurons in the central nervous system, which express a

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Section: Discussionmentioning

confidence: 95%

Endocrine fine-tuning of daily locomotor activity patterns under non-starving conditions in Drosophila

Pauls

Selcho

Raederscheidt

et al. 2020

Preprint

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“…We next sought to determine whether the observed effects of indirect, live yeast exposure were mediated by sight, smell, or taste. Each of these sensory modalities is known to influence aging, physiology, and/or starvation resistance ( 10 , 11 , 17 , 18 ). Smell-blind flies that lack Orco , Ir25a , Ir8a , and Gr63a receptors exhibited a similar increase in starvation resistance when exposed to yeast volatiles compared with the control animals ( Fig.…”

Section: Resultsmentioning

confidence: 99%

“…Octopaminergic neural activity also correlated with fly starvation sensitivity through the regulation of the adipokinetic hormone receptor ( AkhR ) ( 17 ). Starvation-induced sleep loss in Drosophila required octopaminergic neurons, adipokinetic hormone, and the insulin-responsive transcription factor foxo , which influenced the remodeling of small ventral lateral neuron dorsal projections upon nutrient deprivation ( 18 ). Other neuronal populations are known to be activated in response to starvation, including corazonin -expressing neurons, serotonergic neurons, and ellipsoid body R4 neurons ( 19 ).…”

Section: Introductionmentioning

confidence: 99%

Yeast volatiles double starvation survival in Drosophila

et al. 2021

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Organisms make decisions based on the information they gather from their environment, the effects of which affect their fitness. Understanding how these interactions affect physiology may generate interventions that improve the length and quality of life. Here, we provide evidence that exposure to live yeast volatiles during starvation significantly extends survival, increases activity, and slows the rate of triacylglyceride (TAG) decline independent of canonical sensory perception. We demonstrate that ethanol (EtOH) is one of the active components in yeast volatiles that influences these phenotypes and that EtOH metabolites mediate dynamic mechanisms to promote Drosophila survival. Silencing R4d neurons reverses the ability of high EtOH concentrations to promote starvation survival, and their activation promotes EtOH metabolism. The transcription factor foxo promotes EtOH resistance, likely by protection from EtOH toxicity. Our results suggest that food-related cues recruit neural circuits and modulate stress signaling pathways to promote survival during starvation.

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“…70 Wild-type flies increase Akh mRNA levels 3 h after the dark-light or light-dark transition, the time points at which starved flies showed pronounced starvation-induced hyperactivity. 71 Interestingly, times of increased (A-D) Hemolymph sugar levels in Akh>hid,rpr flies and controls: while sucrose and fructose levels did not differ between genotypes and conditions (starved versus fed), trehalose levels were depleted in experimental flies under starvation conditions (p = 0.078 to Gal4/+ and p = 0.063 to UAS/+). In addition, glucose levels were reduced in Akh>hid,rpr flies between fed and starved conditions (p < 0.01), without any effect in control flies (p > 0.05; all N = 3-4).…”

Section: Discussionmentioning

confidence: 98%