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[
Nature,
1992]
Supporters of large DNA sequencing projects will take heart (and find much to learn) from the report by J. Sulston and colleagues that appears on page 37 of this issue. Sulston et al. describe the first results of the Caenorhabditis elegans genome sequencing project, and have come up with not only hitherto unknown genes but also with fresh and biologically relevant information.
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[
Neuron,
2013]
Plasticity models invoke the synaptic delivery of AMPARs, yet we know little about how receptors move invivo. In this issue of Neuron, Hoerndli etal. (2013) show that lateral diffusion and kinesin-mediated transport move AMPARs between synapses invivo.
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[
Nat Cell Biol,
2011]
A potential role for glycosphingolipids and lipid rafts in apical sorting was initially met with enthusiasm, but genetic analysis has since provided little support for it. A report now establishes that glycosphingolipids mediate apical sorting, and specifically help maintain apicobasal polarity in Caenorhabditis elegans.
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[
Cell,
2010]
Most autophagy genes have been discovered in the single-celled yeast Saccharomyces cerevisiae, and little is known about autophagy genes that are specific to multicellular animals. In this issue, Tian et al. (2010) now identify four new autophagy genes: one specific to the nematode Caenorhabditis elegans and three conserved from worms to mammals.
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[
Cell,
2013]
Environmental and cellular cues pattern dendritic growth and direct dendrites to their targets. However, little is known about the signals regulating interactions with the surrounding substrate. Dong etal. and Salzberg etal. now identify a tripartite ligand-receptor complex that conveys cues from the substrate necessary for the patterning of complex dendrites in C.elegans.
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[
Neuron,
2002]
A variety of secreted components have been identified as retrograde signals mediating diverse aspects of synaptic development, maintenance, and plasticity; however, little is known about the mechanisms mediating the release of secreted retrograde signals. Doi and Iwasaki (this issue of Neuron) implicate AEX-1, a protein distantly related to the UNC-13/Munc13 family, as an attractive candidate regulator of the retrograde release machinery in muscle.
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[
Dev Cell,
2002]
Presenilins mediate they-secretase cleavage of Notch transmembrane receptors as well as the transmembrane P-amyloid precursor protein (PAPP), but they are not thought to accomplish this alone. Recent genetic screens in C. elegans, presented in this issue of Developmental Cell, identify two genes that are essential to gamma-secretase activity and may interact with presenilins.
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[
Cell,
1999]
Cell death in universally important in development, not the least in the nervous system, but little is known about how the programmed cell deaths of cells and neurons are ultimately controlled. Much of the understanding of cell death has come from research on the nematode Caenorhabditis elegans (reviewed by Metzstein et al., 1998). Conradt and Horvitz (1999 [this issue of Cell]) now extend this work to provide a satisfyingly complete explanation for the sex-specific death of one particular neuron type in this animal. In so doing, they link up two extensively studied regulatory pathways in C. elegans, one controlling sexual phenotype, and one controlling cell death.
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[
J Cell Biol,
2007]
Cells must break symmetry to acquire polarity. Microtubules have been implicated in the induction of asymmetry in several cell types, but their role in the Caenorhabditis elegans zygote, a classic polarity model, has remained uncertain. One study (see Tsai and Ahringer on p. 397 of this issue) brings new light to this problem by demonstrating that severe loss of microtubules impairs polarity onset in C. elegans.
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[
Science,
1994]
Like people, cells die in different ways: accident, murder, old age, even suicide. In fact, cellular suicide isn't just a curiosity, it's necessary for the health of the organism. During embryonic development, for example, it helps weed out superfluous nerve cells, as well as immune cells that might attack and damage the body's own tissues. Like a spy-plane pilot who carries a little vial of poison under his seat in case he's captured, cells carry in their nuclei a genetic program for suicide that can be set in motion, should the cell receive orders to self-destruct. Now, after years of eluding researchers, the genes that carry out the suicide program are coming into the light...