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Neuron,
2012]
Animals use a form of sensory feedback termed proprioception to monitor their body position and modify the motor programs that control movement. In this issue of Neuron, Wen etal. (2012) provide evidence that a subset of motor neurons function as proprioceptors in C.elegans, where B-type motor neurons sense body curvature to control the bending movements that drive forward locomotion.
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Autophagy,
2007]
Autophagy is a catabolic process in which long-lived proteins and organelles are degraded for recycling in the cytoplasm. In the nematode Caenorhabditis elegans autophagy is associated with formation of the dauer larva, an alternative developmental stage that worms can enter under poor growth conditions. We have shown that C. elegans mutants that experience caloric restriction because they are feeding-defective also exhibit elevated autophagy and decreased levels of fat deposits, as well as smaller cells and, consequently, a smaller body size. Our results suggest novel relationships between caloric restriction, longevity, body size and autophagy.
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Curr Biol,
2014]
Males and females have different evolutionary interests resulting in sexual conflict over optimal life histories. A new study in Caenorhabditis elegans shows that males hijack female physiology after mating to cause body shrinking and, ultimately, death. But how do males benefit from female demise?
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Cell,
2009]
The outgrowth of axons and dendrites from neuronal cell bodies to their appropriate targets is the canonical means of creating new processes. Heiman and Shaham (2009) now show that neuronal processes can also be made by anchoring dendrite tips at their target locations while the cell body pulls away, a process termed retrograde extension.
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Nature,
1996]
Classical results in experimental embryology established long ago that cells of the developing animal have a regional identity. They can be characterized not only as 'skin', 'nerve' and 'bone', but also as 'arm' and 'leg'. But how cells know what body region they belong to, and what to do there, is not known. Results reported in this issue and in Development describe unexpected properties of a key player, one of the Hox genes-the dynamic, lineage-based regulation of a Hox gene in the nematode Caenorhabditis elegans is at odds with a traditional view of Hox genes as relatively fixed markers of regional identity.
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Nature,
2001]
In all animals, the process of programmed cell suicide (apoptosis) is coordinated by enzymes known as caspases, which cut up key substrates in the cell. The dying cell is then neatly packaged, engulfed by neighbouring "phagocytic" cells, and cleared from the body without fanfare, leaving no evidence of the catastrophic events that preceded. It has always been assumed that there is a "point of no return" in this death cascade - at or shortly before the time at which caspases are activated - beyond which the process of cell execution proceeds inexorably. This view is challenged by Reddien et al. and Hoeppner et al. on pages 198 and 202 of this issue. It seems that cells in which caspases have been activated can in fact progress through a state of being "mostly dead", a stage that physically resembles the early phase of apoptosis but from
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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.