Muscle arm development in<i>Caenorhabditis elegans</i>

Dixon, Scott J.; Roy, Peter J.

doi:10.1242/dev.01883

Cited by 64 publications

(85 citation statements)

References 62 publications

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“…We and others suggest that there are two phases of muscle arm development (Dixon and Roy, 2005) (C. R. Norris, I. A. Bazykina, E. M. Hedgecock and D. H. Hall, personal communication).…”

Section: Introductionmentioning

confidence: 81%

“…As the myoblast moves from the nerve cord, muscle membrane remains connected to the nerve cord, resulting in an embryonic muscle arm. By contrast, muscle arm extension during larval development is an active process that requires regulators of the actin cytoskeleton, including ADF/Cofilin (unc-60B) (Dixon and Roy, 2005). It is unknown if microspikes, myopodia, and muscle arms share common regulatory mechanisms.…”

Section: Introductionmentioning

confidence: 99%

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FGF negatively regulates muscle membrane extension inCaenorhabditis elegans

et al. 2006

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Striated muscles from Drosophila and several vertebrates extend plasma membrane to facilitate the formation of the neuromuscular junction (NMJ) during development. However, the regulation of these membrane extensions is poorly understood. In C. elegans, the body wall muscles (BWMs) also have plasma membrane extensions called muscle arms that are guided to the motor axons where they form the postsynaptic element of the NMJ. To investigate the regulation of muscle membrane extension, we screened 871 genes by RNAi for ectopic muscle membrane extensions (EMEs) in C. elegans. We discovered that an FGF pathway, including let-756(FGF), egl-15(FGF receptor), sem-5(GRB2) and other genes negatively regulates plasma membrane extension from muscles. Although compromised FGF pathway activity results in EMEs, hyperactivity of the pathway disrupts larval muscle arm extension, a phenotype we call muscle arm extension defective or MAD. We show that expression of egl-15 and sem-5 in the BWMs are each necessary and sufficient to prevent EMEs. Furthermore, we demonstrate that let-756 expression from any one of several tissues can rescue the EMEs of let-756 mutants, suggesting that LET-756 does not guide muscle membrane extensions. Our screen also revealed that loss-of-function in laminin and integrin components results in both MADs and EMEs, the latter of which are suppressed by hyperactive FGF signaling. Our data are consistent with a model in which integrins and laminins are needed for directed muscle arm extension to the nerve cords, while FGF signaling provides a general mechanism to regulate muscle membrane extension.

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“…We and others suggest that there are two phases of muscle arm development (Dixon and Roy, 2005) (C. R. Norris, I. A. Bazykina, E. M. Hedgecock and D. H. Hall, personal communication).…”

Section: Introductionmentioning

confidence: 81%

Section: Introductionmentioning

confidence: 99%

FGF negatively regulates muscle membrane extension inCaenorhabditis elegans

et al. 2006

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“…Imaging of muscle arms was done using the RP247 strain, expressing the trIs30 transgene (him-4p::MB::YFP; hmr-1b::DsRed2; unc129nsp::DsRed2) (Dixon and Roy, 2005). Imaging was performed using a confocal microscope, and worms were immobilized and orientated using Histoacryl glue (Braun, Tuttingen, Germany).…”

Section: Imagingmentioning

confidence: 99%

Pharmacological assays reveal age-related changes in synaptic transmission at the Caenorhabditis elegans neuromuscular junction that are modified by reduced insulin signalling

Mulcahy

Holden‐Dye

O’Connor

2012

Journal of Experimental Biology

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SUMMARYFrailty is a feature of neuromuscular ageing. Here we provide insight into the relative contribution of pre-and postsynaptic dysfunction to neuromuscular ageing using the nematode Caenorhabditis elegans. Assays of C. elegans motility highlight a precipitous decline during ageing. We describe a novel deployment of pharmacological assays of C. elegans neuromuscular function to resolve pre-and postsynaptic dysfunction that underpin this decreased motility during ageing. The cholinergic agonist levamisole and the cholinesterase inhibitor aldicarb elicited whole worm contraction and allowed a direct comparison of neuromuscular integrity, from 1 to 16days old: measurements could be made from aged worms that were otherwise almost completely immobile. The rapidity and magnitude of the drug-induced contraction provides a measure of neuromuscular signalling whilst the difference between levamisole and aldicarb highlights presynaptic effects. Presynaptic neuromuscular transmission increased between 1 and 5days old in wild-type but not in the insulin/IGF1 receptor mutant daf-2 (e1370). Intriguingly, there was no evidence of a role for insulin-dependent effects in older worms. Notably in 16-day-old worms, which were virtually devoid of spontaneous movement, the maximal contraction produced by both drugs was unchanged. Taken together the data support a maturation of presynaptic function and/or upstream elements during early ageing that is lost after genetic reduction of insulin signalling. Furthermore, this experimental approach has demonstrated a counterintuitive phenomenon: in aged worms neuromuscular strength is maintained despite the absence of motility.

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“…Tropomyosin inhibits actin depolymerizing factor/cofilin activity (Ono and Ono, 2002;Yu and Ono, 2006). Actin depolymerizing factor/cofilin, tropomyosin, and myosin heavy chain are all required for proper muscle arm development (in C. elegans the muscles extend cytoplasmic arms to contact the motor nerves, see third review) (Dixon and Roy, 2005).…”

Section: Thin Filamentmentioning

confidence: 99%

Invertebrate muscles: Thin and thick filament structure; molecular basis of contraction and its regulation, catch and asynchronous muscle

Hooper

Hobbs

Thuma

2008

Progress in Neurobiology

128

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This is the second in a series of canonical reviews on invertebrate muscle. We cover here thin and thick filament structure, the molecular basis of force generation and its regulation, and two special properties of some invertebrate muscle, catch and asynchronous muscle. Invertebrate thin filaments resemble vertebrate thin filaments, although helix structure and tropomyosin arrangement show small differences. Invertebrate thick filaments, alternatively, are very different from vertebrate striated thick filaments and show great variation within invertebrates. Part of this diversity stems from variation in paramyosin content, which is greatly increased in very large diameter invertebrate thick filaments. Other of it arises from relatively small changes in filament backbone structure, which results in filaments with grossly similar myosin head placements (rotating crowns of heads every 14.5 nm) but large changes in detail (distances between heads in azimuthal registration varying from three to thousands of crowns). The lever arm basis of force generation is common to both vetebrates and invertebrates, and in some invertebrates this process is understood on the near atomic level. Invertebrate actomyosin is both thin (tropomyosin:troponin) and thick (primarily via direct Ca ++ binding to myosin) filament regulated, and most invertebrate muscles are dually regulated. These mechanisms are well understood on the molecular level, but the behavioral utility of dual regulation is less so. The phosphorylation state of the thick filament associated giant protein, twitchin, has been recently shown to be the molecular basis of catch. The molecular basis of the stretch activation underlying asynchronous muscle activity, however, remains unresolved.

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Muscle arm development inCaenorhabditis elegans

Cited by 64 publications

References 62 publications

FGF negatively regulates muscle membrane extension inCaenorhabditis elegans

FGF negatively regulates muscle membrane extension inCaenorhabditis elegans

Pharmacological assays reveal age-related changes in synaptic transmission at the Caenorhabditis elegans neuromuscular junction that are modified by reduced insulin signalling

Invertebrate muscles: Thin and thick filament structure; molecular basis of contraction and its regulation, catch and asynchronous muscle

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