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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 ().
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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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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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J Cell Sci,
2004]
Caenorhabditis elegans is a powerful model system for investigating the establishment, regulation and function of adhesive structures in vivo. C elegans has several adhesion complexes related to those in vertebrates. These include: (1) epithelial apical junctions, which have features of both adherens and tight junctions; (2) dense bodies, which are muscle-attachment structures similar to focal adhesions; (3) fibrous organelles, which resemble hemidesmosomes and mediate mechanical coupling between tissues; and (4) a putative dystrophin-glycoprotein complex that has potential roles in muscle function and embryogenesis. Recent work has increased our understanding of these structures and has given new insights into the functions of their vertebrate counterparts.
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Cell,
2015]
Throughout development, proliferative progenitors lose their mitotic potential, exit the cell cycle, and differentiate. In this issue, Ruijtenberg and van den Heuvel identify an important lineage-specific role for a SWI/SNF chromatin-remodeling complex that collaborates with core cell-cycle regulators to promote cell-cycle exit and terminal muscle cell differentiation.
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Curr Biol,
2013]
In the defecation motor program of Caenorhabditis elegans, a pacemaker rhythm generated by the intestine leads to the activation of motor neurons controlling enteric muscle contraction. A new study demonstrates that this signal is conveyed by a neuropeptide that is released from intestinal cells and acutely depolarizes the motorneurons, acting much like a classical neurotransmitter.
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Science,
1998]
Animals use apoptosis, or programmed cell death, to eliminate extraneous or dangerous cells. The muscle of this controlled cellular deconstruction is provided by the caspase family of cysteine proteases, which cleave key targets in the cell. Caspases normally exist in cells as inactive proenzymes; proteolytic processing at a few specific sites unleashes their latent enzymatic activity and triggers cell destruction.