Biology subjects

Faville, R.

Publications and source records attributed to Faville, R..

4 recordsLinked to original sources

bioRxiv2019

{-}{-} Downregulation of a satiety signal from peripheral fat bodies improves visual attention while reducing sleep need in Drosophila .

Sleep is vital for survival. Yet, under environmentally challenging conditions such as starvation, animals suppress their need for sleep. Interestingly, starvation-induced sleep loss does not evoke a subsequent sleep rebound. Little is known about how starvation-induced sleep deprivation differs from other types of sleep loss, or why some sleep functions become dispensable during starvation. Here we demonstrate that downregulation of unpaired-2 (upd2, the Drosophila ortholog of leptin), is sufficient to mimic a starved-like state in flies. We use this genetically starved state to investigate the consequences of a starvation signal on visual attention and sleep in otherwise well-fed flies, thereby sidestepping the negative side-effects of undernourishment. We find that knockdown of upd2 in the fat body is sufficient to suppress sleep while also increasing selective visual attention and promoting night-time feeding. Further, we show that this peripheral signal is integrated in the fly brain via insulin-expressing cells. Together, these findings identify a role for peripheral tissue-to-brain interactions in the simultaneous regulation of sleep and attention, to potentially promote adaptive behaviors necessary for survival in hungry animals.\n\nAuthor SummarySleep is important for maintaining both physiological (e.g., metabolic, immunological, and developmental) and cognitive processes, such as selective attention. Under nutritionally impoverished conditions, animals suppress sleep and increase foraging to locate food. Yet it is currently unknown how an animal is able to maintain well-tuned cognitive processes, despite being sleep deprived. Here we investigate this question by studying flies that have been genetically engineered to lack a satiety signal, and find that signaling from fat bodies in the periphery to insulin-expressing cells in the brain simultaneously regulates sleep need and attention-like processes.

neuroscience↗

bioRxiv2019

Drosophila insulin-like peptide 2 mediates dietary regulation of sleep intensity

Sleep is a nearly universal behavior that is regulated by diverse environmental and physiological stimuli. A defining feature of sleep is a homeostatic rebound following deprivation, where animals compensate for lost sleep by increasing sleep duration and/or sleep depth. Fruit flies exhibit robust recovery sleep following deprivation and represent a powerful model to study neural circuits regulating sleep homeostasis. Numerous neuronal populations have been identified in modulating sleep homeostasis as well as depth, raising the possibility that recovery sleep is differentially regulated by environmental or physiological processes that induce sleep deprivation. Here, we find that unlike most pharmacological and environmental manipulations commonly used to restrict sleep, starvation potently induces sleep loss without a subsequent rebound in sleep duration or depth. We find that both starvation and a sucrose-only diet result in reduced metabolic rate and increased sleep depth, suggesting that dietary yeast protein is essential for normal sleep depth and homeostasis. Finally, we find that Drosophila insulin like peptide 2 (Dilp2) is required for starvation-induced changes in sleep depth without regulating the duration of sleep. Remarkably, Dilp2 mutant flies require rebound sleep following sleep deprivation, suggesting Dilp2 underlies resilience to sleep loss. Together, these findings reveal innate resilience to starvation-induced sleep loss and identify distinct mechanisms that underlie starvation-induced changes in sleep duration and depth.\n\nAuthor SummarySleep is nearly universal throughout the animal kingdom and homeostatic regulation represents a defining feature of sleep, where animals compensate for lost sleep by increasing sleep over subsequent time periods. Despite the robustness of this feature, surprisingly little is known about how recovery-sleep is regulated in response to different types of sleep deprivation. Fruit flies provide a powerful model for investigating the genetic regulation of sleep, and like mammals, display robust recovery sleep following deprivation. Here, we find that unlike most stimuli that suppress sleep, sleep deprivation by starvation does not require a homeostatic rebound. These findings appear to be due to flies engaging in deeper sleep during the period of partial deprivation, suggesting a natural resilience to starvation-induced sleep loss. This unique resilience to starvation-induced sleep loss is dependent on Drosophila insulin-like peptide 2, suggesting a critical role for insulin signaling in regulating interactions between diet and sleep homeostasis.

neuroscience↗

bioRxiv2018

Dopamine D1 receptor signalling differentially regulates action sequences and turning behaviour in freely moving Drosophila

Here, we introduce a novel behavioural paradigm to study neural circuits and mechanisms underlying action selection and decision-making in freely moving Drosophila. We first validate our approach by studying FoxP mutants and show that normally invariant patterns of motor activity and turning behaviour are altered in these flies, reminiscent of indecision. Then, focusing on central complex (CX) circuits known to integrate different sensory modalities and controlling premotor regions, we show that action sequences and turning behaviour are regulated by dopamine D1 (Dop1R1) receptor signalling. Dop1R1 inputs onto CX columnar wedge and ellipsoid body R2/R4m ring neuron circuits both negatively gate motor activity but inversely control turning behaviour. While flies deficient of D1 receptor signalling present normal turning behaviour despite decreased activity, restoring Dop1R1 level in R2/R4m-specific circuitry affects the temporal organisation of motor actions and turning. These findings suggest that columnar wedge and ring neuron circuits of the CX differentially modulate patterns of motor action sequences and turning behaviour by comparative Dop1R1 signalling for goal-directed locomotion.

neuroscience↗

bioRxiv2017

A lineage-related reciprocal inhibition circuitry for sensory-motor action selection

The insect central complex and vertebrate basal ganglia are forebrain centres involved in selection and maintenance of behavioural actions. However, little is known about the formation of the underlying circuits, or how they integrate sensory information for motor actions. Here, we show that paired embryonic neuroblasts generate central complex ring neurons that mediate sensory-motor transformation and action selection in Drosophila. Lineage analysis resolves four ring neuron subtypes, R1-R4, that form GABAergic inhibition circuitry among inhibitory sister cells. Genetic manipulations, together with functional imaging, demonstrate subtype-specific R neurons mediate the selection and maintenance of behavioural activity. A computational model substantiates genetic and behavioural observations suggesting that R neuron circuitry functions as salience detector using competitive inhibition to amplify, maintain or switch between activity states. The resultant gating mechanism translates facilitation, inhibition and disinhibition of behavioural activity as R neuron functions into selection of motor actions and their organisation into action sequences.

neuroscience↗