A subset of sweet-sensing neurons identified by IR56d are necessaryand sufficient for fatty acid taste

Tauber, John M.; Brown, Elizabeth; Li, Yuanyuan; Yurgel, Maria E.; Mašek, Pavel; Keene, Alex C.

doi:10.1101/174623

Cited by 3 publications

(4 citation statements)

References 67 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…In vivo imaging was performed using a previously described protocol with some modifications [89,90]. Briefly, fed, 24-hr–starved, or 3-hr re-fed (standard Bloomington Recipe) flies were anesthetized on ice and secured in a 200-μL pipette tip with head and proboscis accessible.…”

Section: Methodsmentioning

confidence: 99%

A single pair of leucokinin neurons are modulated by feeding state and regulate sleep–metabolism interactions

et al. 2019

Self Cite

View full text Add to dashboard Cite

Dysregulation of sleep and feeding has widespread health consequences. Despite extensive epidemiological evidence for interactions between sleep and metabolic function, little is known about the neural or molecular basis underlying the integration of these processes. D . melanogaster potently suppress sleep in response to starvation, and powerful genetic tools allow for mechanistic investigation of sleep–metabolism interactions. We have previously identified neurons expressing the neuropeptide leucokinin (Lk) as being required for starvation-mediated changes in sleep. Here, we demonstrate an essential role for Lk neuropeptide in metabolic regulation of sleep. The activity of Lk neurons is modulated by feeding, with reduced activity in response to glucose and increased activity under starvation conditions. Both genetic silencing and laser-mediated microablation localize Lk-dependent sleep regulation to a single pair of Lk neurons within the Lateral Horn (LHLK neurons). A targeted screen identified a role for 5′ adenosine monophosphate-activated protein kinase (AMPK) in starvation-modulated changes in sleep. Knockdown of AMPK in Lk neurons suppresses sleep and increases LHLK neuron activity in fed flies, phenocopying the starvation state. Further, we find a requirement for the Lk receptor in the insulin-producing cells (IPCs), suggesting LHLK–IPC connectivity is critical for sleep regulation under starved conditions. Taken together, these findings localize feeding-state–dependent regulation of sleep to a single pair of neurons within the fruit fly brain and provide a system for investigating the cellular basis of sleep–metabolism interactions.

show abstract

Section: Methodsmentioning

confidence: 99%

A single pair of leucokinin neurons are modulated by feeding state and regulate sleep–metabolism interactions

et al. 2019

Self Cite

View full text Add to dashboard Cite

show abstract

“…The Gr64f-expressing taste neurons detect numerous appetitive tastants, including sugars and fatty acids [29][30][31]. While these neurons are activated by both sugars and fatty acids, the response to tastants is conferred by distinct signaling pathways with sugar response dependent on the Gsα subunit [32,33], while fatty acid response is dependent on parallel signaling pathways that include Phospholipase C and Ionotropic Receptor 56d (Ir56d; [29,30,34]). To determine whether aging impairs response to both tastants, we compared the response of young and aged flies to hexanoic acid, a medium-chain fatty acid that robustly activates Gr64f neurons (Fig 1E; [30,31].…”

Section: Resultsmentioning

confidence: 99%

“…Quantifying the ratio of stable mCherry signal to Ca 2+ induced GCaMP6s provides a ratiometric quantification of evoked activity [35][36][37]. We applied an in vivo preparation to record responsiveness of projections in the subesophogeal zone (SEZ) when tastants were applied directly to the proboscis (Fig 2B; [30]). At concentrations ranging from It is also possible that reductions in synaptic innervation of the suboesophageal zone contribute to age-dependent loss of sucrose responsiveness.…”

Section: Resultsmentioning

confidence: 99%

“…Different signaling pathways are responsive to fatty acids and sugars, with sugars activating the cAMP signaling pathway [32] and fatty acids activating the Phospholipase C signaling pathway [34]. To determine whether aging affects the expression of genes associated with either sugar or fatty acid taste perception, we examined genes whose expression has been previously implicated in either of these pathways (Fig 4I , J; [29][30][31][32][33]48,49]. However, there were no significant differences in expression observed in the examined genes with respect to either of these pathways.…”

Section: Resultsmentioning

confidence: 99%

See 1 more Smart Citation

Aging is associated with a modality-specific decline in taste

Brown,

Lloyd,

Martin-Peña

et al. 2024

Preprint

Self Cite

View full text Add to dashboard Cite

Deficits in chemosensory processing are associated with healthy aging, as well as numerous neurodegenerative disorders, including Alzheimer's Disease (AD). In many cases, chemosensory deficits are harbingers of neurodegenerative disease, and understanding the mechanistic basis for these changes may provide insight into the fundamental dysfunction associated with aging and neurodegeneration. The fruit fly,Drosophila melanogaster, is a powerful model for studying chemosensation, aging, and aging-related pathologies, yet the effects of aging and neurodegeneration on chemosensation remain largely unexplored in this model, particularly with respect to taste. To determine whether the effects of aging on taste are conserved in flies, we compared the response of flies to different appetitive tastants. Aging impaired response to sugars, but not medium-chain fatty acids that are sensed by a shared population of neurons, revealing modality-specific deficits in taste. Selective expression of the human amyloid beta (Aβ) 1-42 peptide bearing the Arctic mutation (E693E) associated with early onset AD in the neurons that sense sugars and fatty acids phenocopies the effects of aging, suggesting that the age-related decline in response is localized to gustatory neurons. Functional imaging of gustatory axon terminals revealed reduced response to sugar, but not fatty acids. Axonal innervation of the fly taste center was largely intact in aged flies, suggesting that reduced sucrose response does not derive from neurodegeneration. Conversely, expression of the amyloid peptide in sweet-sensing taste neurons resulted in reduced innervation of the primary fly taste center. A comparison of transcript expression within the sugar-sensing taste neurons revealed age-related changes in 66 genes, including a reduction in odorant-binding protein class genes that are also expressed in taste sensilla. Together, these findings suggest that deficits in taste detection may result from signaling pathway-specific changes, while different mechanisms underly taste deficits in aged and AD model flies. Overall, this work provides a model to examine cellular deficits in neural function associated with aging and AD.

show abstract

Internal amino acid state modulates yeast taste neurons to support protein homeostasis inDrosophila

Steck

Walker

Itskov

et al. 2017

Preprint

View full text Add to dashboard Cite

To optimize fitness, animals must dynamically match food choices to their current needs. For drosophilids, yeast fulfils most dietary protein and micronutrient requirements. While several yeast metabolites activate known gustatory receptor neurons (GRNs) in Drosophila melanogaster, the chemosensory channels mediating yeast feeding remain unknown. Here we identify a class of proboscis GRNs required for yeast intake, and show that these GRNs act redundantly to mediate yeast feeding. While nutritional and reproductive states synergistically increase yeast appetite, we find a separation of these state signals at the level of GRN responses to yeast: amino acid but not mating state enhances yeast GRN gain. The sensitivity of sweet GRNs to sugar is not increased by protein deprivation, providing a potential basis for protein-specific appetite. The emerging picture is that different internal states act at distinct levels of a dedicated gustatory circuit to elicit nutrient-specific appetites towards a complex, ecologically relevant protein source. INTRODUCTIONDecision-making is a key function of the brain. One of the most ancestral and consequential decisions animals need to make is which foods to eat, since balancing the intake of multiple classes of nutrients is critical to optimizing lifespan and reproduction 1 . To do this, many animals, including humans, develop so-called "specific appetites", seeking out and consuming specific foods in response to a physiological deficit of a particular nutrient [2][3][4][5] . Recently, several populations of central neurons driving consumption of specific nutrients have been identified in different species [6][7][8][9] . How these circuits modulate sensory processing to elicit state-specific behavioral responses, however, is poorly understood. The ability to precisely control the intake of dietary proteins is emerging as a conserved phenomenon across phyla. Insects, for example, tightly regulate their intake of protein depending on their internal states 10,11 . Mosquito disease vectors impose a huge burden on human health due to their need for dietary protein, which drives host-seeking and feeding behaviors only during specific internal states 12,13 . Dietary protein homeostasis is not specific to invertebrates, as humans are also able to select highprotein foods when low on protein 14,15 . Although protein is essential for sustaining key physiological processes such as reproduction, excessive protein intake has detrimental effects on aging and health [16][17][18][19][20] . This emphasizes the importance of this tight control of protein intake. Most Drosophila species, including the model organism Drosophila melanogaster, are highly adapted to consume yeast as the major source of non-caloric nutrients in the wild, including proteins, and thus amino acids (AAs) [21][22][23] , as well as sterols, vitamins etc. 24 . It is therefore essential for flies to precisely regulate the intake of yeast. This is achieved by modulating decision-making at different scales, from exploration to fee...

show abstract

A subset of sweet-sensing neurons identified by IR56d are necessaryand sufficient for fatty acid taste

Cited by 3 publications

References 67 publications

A single pair of leucokinin neurons are modulated by feeding state and regulate sleep–metabolism interactions

A single pair of leucokinin neurons are modulated by feeding state and regulate sleep–metabolism interactions

Aging is associated with a modality-specific decline in taste

Internal amino acid state modulates yeast taste neurons to support protein homeostasis inDrosophila

Contact Info

Product

Resources

About