A gene-expression-based neural code for food abundance that modulates lifespan

Entchev, Eugeni V.; Patel, Dhaval; Zhan, Min; Steele, Andrew J.; Lu, Hang; Ch'ng, Quee-Lim

doi:10.7554/elife.06259

Cited by 63 publications

(125 citation statements)

References 67 publications

(149 reference statements)

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“…In C. elegans , food sensory cues influence nearly all aspects of behavior and physiology including sensory functions, locomotion, reproduction, metabolism and lifespan (Lemieux and Ashrafi, 2015; Srinivasan, 2015). Food presence is encoded by two major neuroendocrine systems: serotonin (5-hydroxytryptamine, 5-HT) and transforming growth factor beta (TGF-β) (Entchev et al, 2015). 5-HT synthesis and signaling from a single pair of chemosensory neurons called ADF(L/R) regulates a complex cascade of whole-body metabolic responses that drive peripheral lipid metabolism and fat loss (Srinivasan et al, 2008; Noble et al, 2013).…”

Section: Introductionmentioning

confidence: 99%

C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves

et al. 2016

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SUMMARY It is known that internal physiological state, or interoception, influences central nervous system function and behavior. However, the neurons and mechanisms that integrate sensory information with internal physiological state remain largely unknown. Here, we identify C. elegans body cavity neurons called URX(L/R) as central homeostatic sensors that integrate fluctuations in oxygen availability, with internal metabolic state. We show that depletion of internal body fat reserves increases the tonic activity of URX neurons, which influences the magnitude of the evoked sensory response to oxygen. These responses are integrated via intracellular cGMP and Ca2+. The extent of neuronal activity thus reflects the balance between the perception of oxygen, and available fat reserves. The URX homeostatic sensor ensures that neural signals that stimulate fat loss are only deployed when there are sufficient fat reserves to do so. Our results uncover an interoceptive neuroendocrine axis that relays internal state information to the nervous system.

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Section: Introductionmentioning

confidence: 99%

C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves

et al. 2016

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“…In addition to mouth opening and the induction of pumping, the food signal should also remodel the major developmental pathways regulating the dauer stage: (steroid hormone, TGF-β and insulin) [32, 33]. Presently, we could only speculate how these processes can be activated.…”

Section: Discussionmentioning

confidence: 99%

NAD+ Is a Food Component That Promotes Exit from Dauer Diapause in Caenorhabditis elegans

et al. 2016

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The free-living soil nematode Caenorhabditis elegans adapts its development to the availability of food. When food is scarce and population density is high, worms enter a developmentally arrested non-feeding diapause stage specialized for long-term survival called the dauer larva. When food becomes available, they exit from the dauer stage, resume growth and reproduction. It has been postulated that compound(s) present in food, referred to as the “food signal”, promote exit from the dauer stage. In this study, we have identified NAD+ as a component of bacterial extract that promotes dauer exit. NAD+, when dissolved in alkaline medium, causes opening of the mouth and ingestion of food. We also show that to initiate exit from the dauer stage in response to NAD+ worms require production of serotonin. Thus, C. elegans can use redox cofactors produced by dietary organisms to sense food.

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“…Similar to insulin signaling, nutrient control of TGF‐β/DAF‐7 signaling is likely mediated through regulation of the secreted ligand DAF‐7 whose expression is modulated in response to food‐associated signals . Several regulators of daf‐7 expression have been identified, including positive regulators, heterotrimeric G proteins, GOA‐1, and EGL‐30, and calcium/calmodulin‐dependent protein kinase I (CaMKI/CMK‐1) and the negative regulator Heat Shock Factor‐1 (HSF‐1) .…”

Section: Elegans Respond To Nutrient Limitation By Altering Behavimentioning

confidence: 99%

Nutrient Sensing and Response Drive Developmental Progression in Caenorhabditis elegans

et al. 2020

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In response to nutrient limitation, many animals, including Caenorhabditis elegans, slow or arrest their development. This process requires mechanisms that sense essential nutrients and induce appropriate responses. When faced with nutrient limitation, C. elegans can induce both short and long‐term survival strategies, including larval arrest, decreased developmental rate, and dauer formation. To select the most advantageous strategy, information from many different sensors must be integrated into signaling pathways, including target of rapamycin (TOR) and insulin, that regulate developmental progression. Here, how nutrient information is sensed and integrated into developmental decisions that determine developmental rate and progression in C. elegans is reviewed.

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A gene-expression-based neural code for food abundance that modulates lifespan

Cited by 63 publications

References 67 publications

C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves

C. elegans Body Cavity Neurons Are Homeostatic Sensors that Integrate Fluctuations in Oxygen Availability and Internal Nutrient Reserves

NAD+ Is a Food Component That Promotes Exit from Dauer Diapause in Caenorhabditis elegans

Nutrient Sensing and Response Drive Developmental Progression in Caenorhabditis elegans

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