ArticleThe Journal of neuroscience : the official journal of the Society for Neuroscience2011
Drosophila QVR/SSS modulates the activation and C-type inactivation kinetics of Shaker K(+) channels.
Article in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
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- Waking Up the Sleep Field: An Overview on the Implications of Genetics and Bioinformatics of Sleep.Molecular biotechnology · 2024Review
- Comprehensive insights into the impact of bacterial indole-3-acetic acid on sensory preferences in Drosophila melanogaster.Scientific reports · 2024Article
- ACh Transfers: Homeostatic Plasticity of Cholinergic Synapses.Cellular and molecular neurobiology · 2023Review
- 24-hour urinary potassium excretion is negatively associated with self-reported sleep quality in the general population, independently of sleep-disordered breathing.Journal of clinical sleep medicine : JCSM : official publication of the American Academy of Sleep Medicine · 2022Article
- Lower 24-h urinary potassium excretion is negatively associated with excessive daytime sleepiness in the general population.Sleep & breathing = Schlaf & Atmung · 2022Article
- Constructing and Tuning Excitatory Cholinergic Synapses: The Multifaceted Functions of Nicotinic Acetylcholine Receptors inFrontiers in cellular neuroscience · 2021Review
- The voltage-gated potassium channel Shaker promotes sleep via thermosensitive GABA transmission.Communications biology · 2020Article
- Decreased serum potassium may disturb sleep homeostasis in essential hypertensives.Hypertension research : official journal of the Japanese Society of Hypertension · 2019Article
- Generation and characterization of new alleles of quiver (qvr) that encodes an extracellular modulator of the Shaker potassium channel.Journal of neurogenetics · 2017Article
- Article
- Distinct Mechanisms Underlie Quiescence during Two Caenorhabditis elegans Sleep-Like States.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- Ly6h regulates trafficking of alpha7 nicotinic acetylcholine receptors and nicotine-induced potentiation of glutamatergic signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2015Article
- A neuron-glia interaction involving GABA transaminase contributes to sleep loss in sleepless mutants.Molecular psychiatry · 2015Article
- Aging and Autophagic Function Influences the Progressive Decline of Adult Drosophila Behaviors.PloS one · 2015Article
- SLEEPLESS is a bifunctional regulator of excitability and cholinergic synaptic transmission.Current biology : CB · 2014Article
- Identification of Redeye, a new sleep-regulating protein whose expression is modulated by sleep amount.eLife · 2014Article
- About sleep's role in memory.Physiological reviews · 2013Review
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
Abstract
The quiver/sleepless (qvr/sss) gene encodes a small, glycosylphosphatidylinositol-anchored protein that plays a critical role in the regulation of sleep in Drosophila. Loss-of-function mutations in qvr/sss severely suppress sleep and effect multiple changes in in situ Shaker K(+) currents, including decreased magnitude, slower time-to-peak, and cumulative inactivation. Recently, we demonstrated that SLEEPLESS (SSS) protein modulates Shaker channel activity, possibly through a direct interaction at the plasma membrane. We show here that SSS accelerates the activation of heterologously expressed Shaker channels with no effect on deactivation or fast N-type inactivation. Furthermore, this SSS-induced acceleration is sensitive to the pharmacological disruption of lipid rafts and sufficiently accounts for the slower time-to-peak of in situ Shaker currents seen in qvr/sss mutants. We also find that SSS decreases the rate of C-type inactivation of heterologously expressed Shaker channels, providing a potential mechanism for the cumulative inactivation phenotype induced by qvr/sss loss-of-function mutations. Kinetic modeling based on the in vitro results suggests that the SSS-dependent regulation of channel kinetics accounts for nearly 40% of the decrease in Shaker current magnitude in flies lacking SSS. Sleep duration in qvr/sss-null mutants is restored to normal by a qvr/sss transgene that fully rescues the Shaker kinetic phenotypes but only partially rescues the decrease in current magnitude. Together, these results suggest that the role of SSS in the regulation of sleep in Drosophila correlates more strongly with the effects of SSS on Shaker kinetics than current magnitude.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.