scholarly journals Plant “helper” immune receptors are Ca2+-permeable nonselective cation channels

Science ◽  
2021 ◽  
pp. eabg7917
Author(s):  
Pierre Jacob ◽  
Nak Hyun Kim ◽  
Feihua Wu ◽  
Farid El-Kasmi ◽  
Yuan Chi ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Disease Resistance ◽  
Voltage Clamp ◽  
Cell Voltage ◽  
Cation Channels ◽  
Channel Blockers ◽  
Leucine Rich Repeat ◽  
Nonselective Cation Channels ◽  
Death Signals

Plant nucleotide-binding leucine-rich repeat receptors (NLRs) regulate immunity and cell death. In Arabidopsis, a subfamily of “helper” NLRs are required by many “sensor” NLRs. Active NRG1.1 oligomerized, was enriched in plasma membrane puncta and conferred cytoplasmic Ca2+ influx in plant and human cells. NRG1.1-dependent Ca2+ influx and cell death were sensitive to Ca2+ channel blockers and were suppressed by mutations impacting oligomerization or plasma membrane enrichment. Ca2+ influx and cell death mediated by NRG1.1 and ACTIVATED DISEASE RESISTANCE 1 (ADR1), another “helper” NLR, required conserved negatively charged N-terminal residues. Whole-cell voltage-clamp recordings demonstrate that Arabidopsis “helper” NLRs form Ca2+-permeable cation channels to directly regulate cytoplasmic Ca2+ levels and consequent cell death. Thus, “helper” NLRs transduce cell death signals directly.

Effects of calcium on membrane potential and sodium influx in barnacle muscle fibers

1983 ◽  
Vol 244 (3) ◽  
pp. C297-C302 ◽  
Author(s):  
S. S. Sheu ◽  
M. P. Blaustein
Keyword(s):  
Membrane Potential ◽  
Muscle Fibers ◽  
Cation Channels ◽  
Channel Blockers ◽  
Sodium Influx ◽  
Permeable Channel ◽  
Barnacle Muscle ◽  
Nonselective Cation Channels ◽  
Flux Measurements ◽  
Barnacle Muscle Fibers

The influence of internal and external Ca2+ on membrane potential and 22Na influx were tested in internally perfused giant barnacle muscle fibers. The fibers depolarized by about 2-3 mV, and Na+ influx increased when external Ca2+ was removed. These effects were inhibited and reversed by adding 2 mM La3+ externally but not by tetrodotoxin (TTX). Ca2+ channel blockers did not prevent the depolarization. Increasing internal free Ca2+ ([Ca2+]i) from 10(-7) to 10(-5) M also stimulated Na+ influx and depolarized the fibers by a few millivolts. Neither external La3+ nor TTX prevented the effects of raising [Ca2+]i; however, internal tetrabutylammonium ions depolarized the fibers and attenuated the internal Ca2+-dependent effects. These data are consistent with the idea that removal of external Ca2+ activates a La3+-sensitive channel that is permeable to Na+; raising [Ca2+]i activates a La2+-insensitive, Na+-permeable channel that may be similar to the internal Ca2+-activated nonselective cation channels observed in cardiac muscle. The results demonstrate that all Na+ (and Ca2+) fluxes that do not contribute to Na-Ca exchange must be carefully identified before the exchange stoichiometry can be determined from Na+ and Ca2+ flux measurements.

Non-specific currents at fertilisation in sea urchin oocytes

Zygote ◽  
1998 ◽  
Vol 6 (1) ◽  
pp. 11-15 ◽  
Author(s):  
Maria Laura De Simone ◽  
Lucia Grumetto ◽  
Elisabetta Tosti ◽  
Martin Wilding ◽  
Brian Dale
Keyword(s):  
Plasma Membrane ◽  
Voltage Clamp ◽  
Sea Urchin ◽  
Cell Voltage ◽  
Ion Current ◽  
Inositol Triphosphate ◽  
Whole Cell ◽  
Inward Current ◽  
Voltage Clamp Technique ◽  
Calcium Dependent

SummaryUsing the whole-cell voltage-clamp technique to clamp sea urchin oocytes we show that the fertilising spermatozoon triggers an inward current of −521 ± 56.7 pA (n = 8) at activation. Simultaneously, the plasma membrane depolarises and the conductance increases from 23.4 ± 1.4 to 40.6 ± 1.2 nS (n = 8). The I/V curve for the peak activation current is linear and the current reverses between 0 and + 20 mV, suggesting a non-specific ion current. Since injection of inositol triphosphate induced an inward current of −1062 ± 314 pA (n = 4), and the current was inhibited by preloading oocytes with the calcium chelator BAPTA, the non-specific activation current in sea urchin appears to be calcium dependent.

Muscarinic activation and calcium permeation of nonselective cation currents in airway myocytes

1997 ◽  
Vol 272 (1) ◽  
pp. C341-C349 ◽  
Author(s):  
B. K. Fleischmann ◽  
Y. X. Wang ◽  
M. I. Kotlikoff
Keyword(s):  
Voltage Clamp ◽  
Reversal Potential ◽  
Cation Channels ◽  
Rapid Decline ◽  
Permeability Ratio ◽  
Inward Current ◽  
Physiological Conditions ◽  
Cation Current ◽  
Nonselective Cation Channels ◽  
Instantaneous Voltage

We examined the activation and Ca2+ permeation of nonselective cation channels in voltage-clamped (nystatin), fura 2-loaded equine tracheal myocytes at 35 degrees C. Methacholine (50 microM) induced a biphasic increase in intracellular Ca2+ concentration ([Ca2+]i) and a biphasic inward current consisting of a large, rapidly inactivating Ca(2+)-activated Cl current [ICl(Ca)] and a smaller, sustained nonselective cation current (Icat) ICl(Ca) but not Icat was activated by caffeine. Neither Icat nor the sustained rise in [Ca2+]i was blocked by nisoldipine, whereas both were rapidly blocked by Ni2+; Icat was determined to be Ca2+ permeant, since 1) a sustained elevation of [Ca2+]i occurred when Icat was activated, and blockade of Icat produced a rapid decline in [Ca2+]i; 2) increasing extracellular Ca2+ during Icat increased [Ca2+]i; 3) 110 mM extracellular Ca2+ shifted the reversal potential of Icat to 12 mV (Ca(2+)-to-Cs+ permeability ratio = 3.6); and 4) instantaneous voltage-clamp steps to negative potentials during Icat increased the current and [Ca2+]i, whereas depolarizing steps decreased the current and [Ca2+]i. The fraction of Icat carried by Ca2+ under physiological conditions was estimated to be 14% at -60 mV.

scholarly journals Plant NLR targets P-type ATPase for executing plasma membrane depolarization leading to calcium influx and cell death

2020 ◽  
Author(s):  
Hye-Young Lee ◽  
Ye-Eun Seo ◽  
Joo Hyun Lee ◽  
So Eui Lee ◽  
Soohyun Oh ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Calcium Influx ◽  
Coiled Coil ◽  
Membrane Depolarization ◽  
Leucine Rich Repeat ◽  
Primary Target ◽  
Robust Immune Response ◽  
Hr Cell Death ◽  
P Type

AbstractHypersensitive response (HR) is a robust immune response mediated by plant nucleotide-binding and leucine-rich repeat receptor (NLR). However, the early molecular event linking NLR to cell death is obscure. Here we demonstrate that NLR targets plasma membrane H+-ATPases (PMA) generating electrochemical potential across the membrane. CCA309, an autoactive N-terminal domain of pepper coiled-coil NLR (CNL), associates with PMAs and its autoactivity is affected by silencing or overexpression of PMA. CCA309-induced extracellular alkalization accompanied with membrane depolarization is followed by calcium influx and cell death. CCA309 interacts with C-terminal regulatory domain of PMA and 14-3-3 negatively affects CCA309-induced cell death. Moreover, pharmacological experiments with fusicoccin, an irreversible PMA activator, confirmed that CC- and CNL-mediated cell death occurred through inhibiting PMA. We propose PMAs as the primary target of plasma membrane-associated CNL to disrupt electrochemical homeostasis leading to HR cell death.

Nonselective cation channels coupled with tachykinin receptors in rat sensory neurons

1995 ◽  
Vol 73 (2) ◽  
pp. 736-742 ◽  
Author(s):  
K. Inoue ◽  
K. Nakazawa ◽  
K. Inoue ◽  
K. Fujimori
Keyword(s):  
Sensory Neurons ◽  
Reversal Potential ◽  
Cell Voltage ◽  
Cation Channels ◽  
Neurokinin A ◽  
Extracellular Solution ◽  
Inward Current ◽  
Nonselective Cation Channels ◽  
Excitatory Neurotransmission ◽  
In Cells

1. Effects of substance P (SP) and other tachykinins on membrane currents were investigated using whole cell voltage clamp in cultured sensory neurons isolated from rat dorsal root ganglia. 2. SP (100 nM) evoked an inward current in two-thirds of the cells at negative potentials. In most of the cells that generated the inward current in response to SP, capsaicin also activated an inward current. The SP-evoked inward current was not observed in cells loaded with 2 mM guanosine 5'-O-(2-thiodiphosphate) (GDP beta S). 3. Neurokinin A (NKA) or neurokinin B (NKB) also activated an inward current. At 100 nM of each agonist, the order was NKB > NKA > SP with respect to activated current amplitude. 4. The tachykinin-activated current was reversed around +10 mV with a standard extracellular solution containing 140 mM NaCl. The reversal potential became more negative when extracellular NaCl was reduced by substituting with sucrose. The inward current was also activated in cells bathed in an extracellular solution containing Cs+, tetraethylammonium (TEA) or N-methyl-D-glucamine (NMDG) as a major cation instead of Na+. The order of permeability, determined from the reversal potential of the current, was Cs+ not equal to Na+ > TEA > NMDG. The amplitude of the inward current activated by NKB was increased when extracellular Na+ was replaced with Cs+, TEA or NMDG. 5. Permeability of Ca2+ was tested using an extracellular solution containing Ca2+ as the only cation (111.8 mM Ca2+ outside). Under this condition, NKB evoked an inward current that reversed around +30 mV. 6. The results suggest that SP and other tachykinins activate nonselective cation channels, which are also permeable to Ca2+, through receptors which are more responsive to NKB than to SP or NKA. The channel activation may serve as a mechanism underlying tachykinin-mediated excitatory neurotransmission in sensory neurons.

scholarly journals A trimeric CrRLK1L-LLG1 complex genetically modulates SUMM2-mediated autoimmunity

2020 ◽  
Vol 11 (1) ◽  
Author(s):  
Yanyan Huang ◽  
Chuanchun Yin ◽  
Jun Liu ◽  
Baomin Feng ◽  
Dongdong Ge ◽  
...  
Keyword(s):  
Cell Death ◽  
Plasma Membrane ◽  
Catharanthus Roseus ◽  
Nucleotide Binding ◽  
Mapk Cascade ◽  
Leucine Rich Repeat ◽  
Mapk Kinase ◽  
Trimeric Complex ◽  
Cell Death Pathway ◽  
Receptor Like Kinase

Abstract Cell death is intrinsically linked with immunity. Disruption of an immune-activated MAPK cascade, consisting of MEKK1, MKK1/2, and MPK4, triggers cell death and autoimmunity through the nucleotide-binding leucine-rich repeat (NLR) protein SUMM2 and the MAPK kinase kinase MEKK2. In this study, we identify a Catharanthus roseus receptor-like kinase 1-like (CrRLK1L), named LETUM2/MEDOS1 (LET2/MDS1), and the glycosylphosphatidylinositol (GPI)-anchored protein LLG1 as regulators of mekk1-mkk1/2-mpk4 cell death. LET2/MDS1 functions additively with LET1, another CrRLK1L, and acts genetically downstream of MEKK2 in regulating SUMM2 activation. LET2/MDS1 complexes with LET1 and promotes LET1 phosphorylation, revealing an intertwined regulation between different CrRLK1Ls. LLG1 interacts with the ectodomain of LET1/2 and mediates LET1/2 transport to the plasma membrane, corroborating its function as a co-receptor of LET1/2 in the mekk1-mkk1/2-mpk4 cell death pathway. Thus, our data suggest that a trimeric complex consisting of two CrRLK1Ls LET1, LET2/MDS1, and a GPI-anchored protein LLG1 that regulates the activation of NLR SUMM2 for initiating cell death and autoimmunity.

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