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Transient stripping of subducting slabs controls periodic forearc uplift.

ABSTRACT: Topography in forearc regions reflects tectonic processes along the subduction interface, from seismic cycle-related transients to long-term competition between accretion and erosion. Yet, no consensus exists about the topography drivers, especially as the contribution of deep accretion remains poorly constrained. Here, we use thermo-mechanical simulations to show that transient slab-top stripping events at the base of the forearc crust control uplift-then-subsidence sequences. This 100s-m-high topographic signal with a Myr-long periodicity, mostly inaccessible to geodetic and geomorphological records, reflects the nature and influx rate of material involved in the accretion process. The protracted succession of stripping events eventually results in the pulsing rise of a large, positive coastal topography. Trench-parallel alternation of forearc highs and depressions along active margins worldwide may reflect temporal snapshots of different stages of these surface oscillations, implying that the 3D shape of topography enables tracking deep accretion and associated plate-interface frictional properties in space and time.

SUBMITTER: Menant A

PROVIDER: S-EPMC7156703 | biostudies-literature | 2020 Apr

REPOSITORIES: biostudies-literature

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Transient stripping of subducting slabs controls periodic forearc uplift.

Menant Armel A Angiboust Samuel S Gerya Taras T Lacassin Robin R Simoes Martine M Grandin Raphael R

Nature communications 20200414 1

Topography in forearc regions reflects tectonic processes along the subduction interface, from seismic cycle-related transients to long-term competition between accretion and erosion. Yet, no consensus exists about the topography drivers, especially as the contribution of deep accretion remains poorly constrained. Here, we use thermo-mechanical simulations to show that transient slab-top stripping events at the base of the forearc crust control uplift-then-subsidence sequences. This 100s-m-high ...[more]

PMID: 32286304

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Project description:We studied a two-generation family presenting with conditions that included progressive permanent weakness, myopathic myopathy, exercise-induced contracture before normokalaemic periodic paralysis or, if localized to the tibial anterior muscle group, transient compartment-like syndrome (painful acute oedema with neuronal compression and drop foot). 23Na and 1H magnetic resonance imaging displayed myoplasmic sodium overload, and oedema. We identified a novel familial Ca(v)1.1 calcium channel mutation, R1242G, localized to the third positive charge of the domain IV voltage sensor. Functional expression of R1242G in the muscular dysgenesis mouse cell line GLT revealed a 28% reduced central pore inward current and a -20 mV shift of the steady-state inactivation curve. Both changes may be at least partially explained by an outward omega (gating pore) current at positive potentials. Moreover, this outward omega current of 27.5 nS/nF may cause the reduction of the overshoot by 13 mV and slowing of the upstroke of action potentials by 36% that are associated with muscle hypoexcitability (permanent weakness and myopathic myopathy). In addition to the outward omega current, we identified an inward omega pore current of 95 nS/nF at negative membrane potentials after long depolarizing pulses that shifts the R1242G residue above the omega pore constriction. A simulation reveals that the inward current might depolarize the fibre sufficiently to trigger calcium release in the absence of an action potential and therefore cause an electrically silent depolarization-induced muscle contracture. Additionally, evidence of the inward current can be found in 23Na magnetic resonance imaging-detected sodium accumulation and 1H magnetic resonance imaging-detected oedema. We hypothesize that the episodes are normokalaemic because of depolarization-induced compensatory outward potassium flux through both delayed rectifiers and omega pore. We conclude that the position of the R1242G residue before elicitation of the omega current is decisive for its conductance: if the residue is located below the gating pore as in the resting state then outward currents are observed; if the residue is above the gating pore because of depolarization, as in the inactivated state, then inward currents are observed. This study shows for the first time that functional characterization of omega pore currents is possible using a cultured cell line expressing mutant Ca(v)1.1 channels. Likewise, it is the first calcium channel mutation for complicated normokalaemic periodic paralysis.

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Transient stripping of subducting slabs controls periodic forearc uplift.

Publications

Transient stripping of subducting slabs controls periodic forearc uplift.

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