Alternative splicing of the muscarinic acetylcholine receptor GAR-3 in

Park, Yang-Seo; Kim, Seungwoo; Shin, Youngju; Choi, Boram; Cho, Nam Jeong

doi:10.1016/s0006-291x(03)01508-0

Cited by 27 publications

(30 citation statements)

References 17 publications

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“…Actions of acetylcholine on neurons and muscles of C. elegans are the result of activation not only nAChRs, but also metabotropic muscarinic acetylcholine receptors (mAChRs) (Kim et al, 2008;Lee et al, 2000;Liu et al, 2007;Park et al, 2003;Steger & Avery, 2004). In order to determine the possible role of mAChRs in the behavior thermotolerance we tested the influence of agonists of these receptors on the ability of C. elegans to maintain swimming, induced by mechanical stimulus at extreme high temperature 36 °C.…”

Section: Resultsmentioning

confidence: 99%

“…The C. elegans genome encodes three mAChRs, GAR-1, GAR-2 and GAR-3 (Kim et al, 2008;Lee et al, 2000;Liu et al, 2007;Park et al, 2003;Steger & Avery, 2004). All of them show high similarity in amino acids sequences to the known mammalian mAChRs M 1 , M 2 , M 3 , M 4 and M 5 , which are coupled to different G-proteins (Caulfield & Birdsall, 1998;Langmead et al, 2008;Lanzafame et al, 2003).…”

Section: (Ok755) Gar-2(ok520) and Gar-3(vu78)mentioning

confidence: 99%

“…Acetylcholine (ACh) is the major neurotransmitter not only in vertebrates but also in the simple organism of soil nematode Caenorhabditis elegans and more than one third of neurons in C. elegans nervous system release ACh. In C. elegans molecular mechanisms of ACh effects on postsynaptic neurons and muscles are similar with such in mammals and are realized by ACh binding with either nicotinic or muscarinic receptors (Changeux & Edelstein, 1998;Fleming, et al, 1997;Kim, Shin, Park, & Cho, 2008;Lee et al, 2000;Liu, LeBoeuf, & Garcia, 2007;Park, Kim, Shin, Choi, & Cho, 2003;Satelle, 2009;Steger & Avery, 2004). Nicotinic receptors (nAChRs) are ligand-gated ion channels and responsible for the initial fast depolarization in the postsynaptic neurons and muscles (Changeux & Edelstein, 1998;Culetto et al, 2004;Satelle, 2009;Unwin, 2005).…”

Section: Introductionmentioning

confidence: 99%

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Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Kalinnikova¹,

Шагидуллин²,

Колсанова³

et al. 2013

ENRR

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The nervous system is a target of hyperthermic failure of animal behavior. Caenorhabditis elegans can be used as an excellent model organism to investigate mechanisms underlying thermotolerance of nervous system. Inhibition of ACh-esterase by neostigmine produces rise in thermotolerance of C. elegans swimming induced by mechanical stimulus at constant temperature 36 °C. Protection of C. elegans behavior against heat stress by neostigmine indicates that hyperthermia induces ACh deficiency in the C. elegans nervous system which is one of the causes of hyperthermic failure of behavior. Activation of mAChRs by pilocarpine or oxotremorine M elevates behavior thermotolerance similarly with neostigmine while inhibition of these receptors by atropine has opposite effect. These results suggest that ACh protects C. elegans behavior against hyperthermia by binding with mAChRs. It is known that three G-protein coupled ACh receptors of C. elegans (GAR-1, GAR-2 and GAR-3) have sequence homology with five known subtypes of mammalian mAChRs. To identify mAChRs responsible for regulation of behavior response to hyperthermia we investigated effects of loss-of-function mutations in gar-1, gar-2 and gar-3 genes on the sensitivity of behavior thermotolerance to neostigmine and pilocarpine. Among them only loss-of-function gar-3 mutation caused insensitivity of C. elegans behavior thermotolerance to neostigmine and pilocarpine. Thus it is GAR-3 mAChR that mediates rise in behavior thermotolerance produced by ACh-esterase inhibitor neostigmine or agonists of mammalian mAChRs.

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Section: Resultsmentioning

confidence: 99%

Section: (Ok755) Gar-2(ok520) and Gar-3(vu78)mentioning

confidence: 99%

Section: Introductionmentioning

confidence: 99%

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Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Kalinnikova¹,

Шагидуллин²,

Колсанова³

et al. 2013

ENRR

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“…In contrast to mammalian mAChRs, pharmacological studies using cultured cells showed that of the three C. elegans mAChRs, only GAR-3 is activated by oxotremorine, a derivative of oxotremorine M Lee et al, 1999Lee et al, , 2000Park et al, 2000Park et al, , 2006. In Chinese hamster ovary cell culture, GAR-3(mAChR) has been shown to activate PLC, which is a downstream effector of G␣ q signaling (Park et al, 2003). Loss-of-function gar-3 mutants are grossly normal in behaviors.…”

Section: Machr Gar-3 Activates G␣ Q In Regulating Spicule Protractionmentioning

confidence: 99%

Gα_q-Coupled Muscarinic Acetylcholine Receptors Enhance Nicotinic Acetylcholine Receptor Signaling inCaenorhabditis elegansMating Behavior

Liu¹,

LeBoeuf²,

García³

2007

J. Neurosci.

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In this study, we address why metabotropic and ionotropic cholinergic signaling pathways are used to facilitate motor behaviors. We demonstrate that a G␣ q -coupled muscarinic acetylcholine receptor (mAChR) signaling pathway enhances nicotinic acetylcholine receptor (nAChR) signaling to facilitate the insertion of the Caenorhabditis elegans male copulatory spicules into the hermaphrodite during mating. Previous studies showed that ACh (acetylcholine) activates nAChRs on the spicule protractor muscles to induce the attached spicules to extend from the tail. Using the mAChR agonist Oxo M (oxotremorine M), we identified a GAR-3(mAChR)-G␣ q pathway that promotes protractor muscle contraction by upregulating nAChR signaling before mating. GAR-3(mAChR) is expressed in the protractor muscles and in the spicule-associated SPC and PCB cholinergic neurons. However, ablation of these neurons or impairing cholinergic transmission reduces drug-induced spicule protraction, suggesting that drug-stimulated neurons directly activate muscle contraction. Behavioral analysis of gar-3 mutants indicates that, in wild-type males, GAR-3(mAChR) expression in the SPC and PCB neurons is required for the male to sustain rhythmic spicule muscle contractions during attempts to breach the vulva. We propose that the GAR-3(mAChR)/G␣ q pathway sensitizes the spicule neurons and muscles before and during mating so that the male can respond to hermaphrodite vulva efficiently.

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“…Since GAR-3-mediated PLC stimulation is not affected by PTX treatment (Park et al 2003), it is likely that the PLC-dependent ERK1/2 activation occurs through PTX-insensitive Gq proteins. It has been reported, however, that mammalian mAChRs can couple to both PTX-insensitive and -sensitive G proteins for ERK activation (Crespo et al 1994;Wotta et al 1998;Wylie et al 1999).…”

Section: Gar-3 Activates Erk1/2 In a Ptx-sensitive Mannermentioning

confidence: 99%

ERK1/2 activation by theC. elegansmuscarinic acetylcholine receptor GAR-3 in cultured mammalian cells involves multiple signaling pathways

Shin

Kim

et al. 2010

Animal Cells and Systems

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Extracellular signal-regulated kinases 1/2 (ERK1/2) play important roles in a variety of biological processes including cell growth and differentiation. We have previously reported that GAR-3 activates ERK1/2 via phospholipase C and protein kinase C, presumably through pertussis toxin (PTX)-insensitive Gq proteins, in Chinese hamster ovary (CHO) cells. Here we provide evidence that GAR-3 also activates ERK1/2 through PTX-sensitive G proteins, phosphatidylinositol 3-kinase (PI 3-kinase), and Src family kinases in CHO cells. We further show that in human embryonic kidney (HEK293) cells, epidermal growth factor receptor and Ras are required for efficient ERK1/2 activation by GAR-3. Taken together, our data indicate that GAR-3 evokes ERK1/2 activation through multiple signaling pathways in cultured mammalian cells.

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Alternative splicing of the muscarinic acetylcholine receptor GAR-3 in

Cited by 27 publications

References 17 publications

Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Gα_q-Coupled Muscarinic Acetylcholine Receptors Enhance Nicotinic Acetylcholine Receptor Signaling inCaenorhabditis elegansMating Behavior

ERK1/2 activation by theC. elegansmuscarinic acetylcholine receptor GAR-3 in cultured mammalian cells involves multiple signaling pathways

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Alternative splicing of the muscarinic acetylcholine receptor GAR-3 in

Cited by 27 publications

References 17 publications

Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Acetylcholine Deficiency in Caenorhabditis elegans Induced by Hyperthermia Can Be Compensated by ACh-esterase Inhibition or Activation of GAR-3 mAChRs

Gαq-Coupled Muscarinic Acetylcholine Receptors Enhance Nicotinic Acetylcholine Receptor Signaling inCaenorhabditis elegansMating Behavior

ERK1/2 activation by theC. elegansmuscarinic acetylcholine receptor GAR-3 in cultured mammalian cells involves multiple signaling pathways

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Gα_q-Coupled Muscarinic Acetylcholine Receptors Enhance Nicotinic Acetylcholine Receptor Signaling inCaenorhabditis elegansMating Behavior