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Julien Hering – One of the best experts on this subject based on the ideXlab platform.

  • Slow Inactivation of the CaV3.1 isotype of T- type calcium channels.
    The Journal of Physiology, 2004
    Co-Authors: Julien Hering, Anne Feltz, Régis C. Lambert
    Abstract:

    T-type calcium channels (the CaV3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat CaV3.1 channel and whole-cell voltvoltage clamclamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V0.5) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

  • Slow Inactivation of the Ca(V)3.1 isotype of T-type calcium channels.
    Journal of Physiology – Paris, 2004
    Co-Authors: Julien Hering, Anne Feltz, R.c. Lambert
    Abstract:

    T-type calcium channels (the Ca(V)3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat Ca(V)3.1 channel and whole-cell voltvoltage clamclamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (tau= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V(0.5)) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

Régis C. Lambert – One of the best experts on this subject based on the ideXlab platform.

  • Slow Inactivation of the CaV3.1 isotype of T- type calcium channels.
    The Journal of Physiology, 2004
    Co-Authors: Julien Hering, Anne Feltz, Régis C. Lambert
    Abstract:

    T-type calcium channels (the CaV3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat CaV3.1 channel and whole-cell voltage clamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V0.5) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

Gary Ruvkun – One of the best experts on this subject based on the ideXlab platform.

  • lysosomal activity regulates caenorhabditis elegans mitochondrial dynamics through vitamin b12 metabolism
    Proceedings of the National Academy of Sciences of the United States of America, 2020
    Co-Authors: Wei Wei, Gary Ruvkun
    Abstract:

    Mitochondrial fission and fusion are highly regulated by energy demand and physiological conditions to control the production, activity, and movement of these organelles. Mitochondria are arrayed in a periodic pattern in Caenorhabditis elegans muscle, but this pattern is disrupted by mutations in the mitochondrial fission component dynamin DRP-1. Here we show that the dramatically disorganized mitochondria caused by a mitochondrial fission-defective dynamin mutation is strongly suppressed to a more periodic pattern by a second mutation in lysosomal biogenesis or acidification. Vitamin B12 is normally imported from the bacterial diet via lysosomal degradation of B12-binding proteins and transport of vitamin B12 to the mitochondrion and cytoplasm. We show that the lysosomal dysfunction induced by gene Inactivations of lysosomal biogenesis or acidification factors causes vitamin B12 deficiency. Growth of the C. elegans dynamin mutant on an Escherichia coli strain with low vitamin B12 also strongly suppressed the mitochondrial fission defect. Of the two C. elegans enzymes that require B12, gene Inactivation of methionine synthase suppressed the mitochondrial fission defect of a dynamin mutation. We show that lysosomal dysfunction induced mitochondrial biogenesis, which is mediated by vitamin B12 deficiency and methionine restriction. S-adenosylmethionine, the methyl donor of many methylation reactions, including histones, is synthesized from methionine by S-adenosylmethionine synthase; Inactivation of the sams-1 S-adenosylmethionine synthase also suppresses the drp-1 fission defect, suggesting that vitamin B12 regulates mitochondrial biogenesis and then affects mitochondrial fission via chromatin pathways.

  • lysosomal activity regulates caenorhabditis elegans mitochondrial dynamics through vitamin b12 metabolism
    bioRxiv, 2020
    Co-Authors: Wei Wei, Gary Ruvkun
    Abstract:

    Mitochondrial fission and fusion are highly regulated by energy demand and physiological conditions to control the production, activity, and movement of these organelles. Mitochondria are arrayed in a periodic pattern in Caenorhabditis elegans muscle, but this pattern is disrupted by mutations in the mitochondrial fission component dynamin. Here we show that the dramatically disorganized mitochondria caused by a mitochondrial fission-defective dynamin mutation is strongly suppressed to a more periodic pattern by a second mutation in lysosomal biogenesis or acidification. Vitamin B12 is normally imported from the bacterial diet via lysosomal degradation of B12-binding proteins and transport of vitamin B12 to the mitochondrion and cytoplasm. We show that the lysosomal dysfunction induced by gene Inactivations of lysosomal biogenesis or acidification factors causes vitamin B12 deficiency. Growth of the C. elegans dynamin mutant on an E. coli strain with low vitamin B12 also strongly suppressed the mitochondrial fission defect. Of the two C. elegans enzymes that require B12, gene Inactivation of methionine synthase suppressed the mitochondrial fission defect of a dynamin mutation. We show that lysosomal dysfunction induced mitochondrial biogenesis which is mediated by vitamin B12 deficiency and methionine restriction. S-adenosylmethionine, the methyl donor of many methylation reactions, including histones, is synthesized from methionine by S-adenosylmethionine synthase; Inactivation of the sams-1 S-adenosylmethionine synthase also suppresses the drp-1 fission defect, suggesting that vitamin B12 regulates mitochondrial biogenesis and then affects mitochondrial fission via chromatin pathways.

  • Lifespan regulation by evolutionarily conserved genes essential for viability
    PLoS Genetics, 2007
    Co-Authors: Sean P. Curran, Gary Ruvkun
    Abstract:

    Evolutionarily conserved mechanisms that control aging are predicted to have prereproductive functions in order to be subject to natural selection. Genes that are essential for growth and development are highly conserved in evolution, but their role in longevity has not previously been assessed. We screened 2,700 genes essential for Caenorhabditis elegans development and identified 64 genes that extend lifespan when inactivated postdevelopmentally. These candidate lifespan regulators are highly conserved from yeast to humans. Classification of the candidate lifespan regulators into functional groups identified the expected insulin and metabolic pathways but also revealed enrichment for translation, RNA, and chromatin factors. Many of these essential gene Inactivations extend lifespan as much as the strongest known regulators of aging. Early gene Inactivations of these essential genes caused growth arrest at larval stages, and some of these arrested animals live much longer than wild-type adults. daf-16 is required for the enhanced survival of arrested larvae, suggesting that the increased longevity is a physiological response to the essential gene Inactivation. These results suggest that insulin-signaling pathways play a role in regulation of aging at any stage in life.

R.c. Lambert – One of the best experts on this subject based on the ideXlab platform.

  • Slow Inactivation of the Ca(V)3.1 isotype of T-type calcium channels.
    Journal of Physiology – Paris, 2004
    Co-Authors: Julien Hering, Anne Feltz, R.c. Lambert
    Abstract:

    T-type calcium channels (the Ca(V)3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat Ca(V)3.1 channel and whole-cell voltage clamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (tau= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V(0.5)) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

Anne Feltz – One of the best experts on this subject based on the ideXlab platform.

  • Slow Inactivation of the CaV3.1 isotype of T- type calcium channels.
    The Journal of Physiology, 2004
    Co-Authors: Julien Hering, Anne Feltz, Régis C. Lambert
    Abstract:

    T-type calcium channels (the CaV3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat CaV3.1 channel and whole-cell voltage clamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V0.5) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.

  • Slow Inactivation of the Ca(V)3.1 isotype of T-type calcium channels.
    Journal of Physiology – Paris, 2004
    Co-Authors: Julien Hering, Anne Feltz, R.c. Lambert
    Abstract:

    T-type calcium channels (the Ca(V)3 channel family) are involved in defining the resting membrane potential and in neuronal activities such as oscillations and rebound depolarization. Their physiological roles depend upon the channel activation and Inactivation kinetics. A fast Inactivation that stops the ionic flux of calcium in tens of milliseconds has already been described in both native and heterologously expressed channels. Here, using HEK 293 cells expressing the rat Ca(V)3.1 channel and whole-cell voltage clamp, we investigate an additional Inactivation process, which can be distinguished from the previously described fast Inactivation by its slow time course of recovery from Inactivation (tau= 1 s) and by its sensitivity to external calcium. Steady-state slow Inactivation is voltage dependent around the resting membrane potential (the potential of half-Inactivation (V(0.5)) =-70 mV, slope factor = 7.4 mV) and can reduce the calcium current by up to 50%. Near resting potential, the slow Inactivation displays a half-time of induction of tens of seconds. The slow Inactivation therefore modulates the availability of T-type calcium channels depending upon recent cell history, providing a mechanism to store information in a time scale of seconds.