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Dev Cell,
2015]
Sensory neurons interact with muscles in many contexts, but muscle-derived signals that pattern sensory dendrites have not been extensively characterized. In this issue of Developmental Cell, Liang etal. (2015) report a signaling system in which positional cues from muscle are transduced to hypodermal cells to direct sensory dendrite outgrowth.
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Worm,
2016]
Locomotion of C. elegans requires coordinated, efficient transmission of forces generated on the molecular scale by myosin and actin filaments in myocytes to dense bodies and the hypodermis and cuticle enveloping body wall muscles. The complex organization of the acto-myosin scaffold with its accessory proteins provides a fine-tuned machinery regulated by effectors that guarantees that sarcomere units undergo controlled, reversible cycles of contraction and relaxation. Actin filaments in sarcomeres dynamically undergo polymerization and depolymerization. In a recent study, the actin-binding protein DBN-1, the C. elegans ortholog of human drebrin and drebrin-like proteins, was discovered to stabilize actin in muscle cells. DBN-1 reversibly changes location between actin filaments and myosin-rich regions during muscle contraction. Mutations in DBN-1 result in mislocalization of other actin-binding proteins. Here we discuss implications of this finding for the regulation of sarcomere actin stability and the organization of other actin-binding proteins.
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J Cardiovasc Aging,
2023]
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[
Cell,
2008]
Muscle contractions are driven by neurotransmitters released at neuromuscular junctions. In this issue, Beg et al. (2008) report that protons, in the absence of neurotransmitters and neurons, can stimulate muscle contractions involved in the defecation cycle of the worm Caenorhabditis elegans. Their results identify protons as a new intercellular messenger and suggest that proton-mediated intercellular communication may be a widespread phenomenon.
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Nature,
2002]
Detailed studies of cellular changes in ageing nematode worms show that they, like humans, suffer progressive muscle deterioration. Randomness of cell damage is another shared hallmark of the ageing process.
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Nature,
1996]
Springtime finds hopeful anglers baiting hungry fish with twitching worms, both live and artificial. Fish prefer the large annelids, but Kemp and coworkers have knotted on their lines the small, alluring nematode Caenorhabditis elegans, which twitches spasmodically when the aptly named protein twitchin goes missing from its muscle cells. And they've caught a big one! On page 636 of this issue, these authors report that the giant protein kinase twitchin, which has a relative molecular mass of 750K and is found in nematode muscle cells, and the protein S100A1(2), a member of the S100 family of calcium-binding proteins, make up a third new calcium-regulated system in muscle which may be of great importance in organizing muscle structure and maintaining its resting tension. They show that a fragment of twitchin containing the autoinhibited kinase domain is specifically activated in a calcium-dependent and zinc-enhanced manner by S100A1(2), but not by the S100B(2) isoform with which it shares 60 percent homology....
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Curr Biol,
2011]
Lamin mutations cause muscular dystrophies, but the mechanism is unclear. Anew study shows that lamin mutant worms display muscle-specific defects linked to altered subnuclear localization of heterochromatin, leading to altered gene expression.
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Nat Neurosci,
2003]
A new study in this issue demonstrates that two GABAergic motor neurons in C. elegans are excitatory at target muscles because GABA activates a ligand-gated cation conductance, which is structurally similar to several other ligand-gated channels.
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Cell Metab,
2006]
What are the pathways that underlie the coordinated responses of an organism to well-fed and food-deprived states? A report in this issue of Cell Metabolism suggests that starvation functions via a muscarinic acetylcholine receptor to activate MAP kinase signaling in the pharyngeal muscle of C. elegans ().