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[
Cell Cycle,
2011]
Comment on: Banerjee D, et al. Cell Cycle 2010; 9:4748-65.
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[
Nat Cell Biol,
2010]
Recognition of apoptotic cells by phagocytic cells in Caenorhabditis elegans has been something of a mystery. A secreted transthyretin-like protein, TTR-52, has been identified as a bridging molecule between apoptotic cells and CED-1 on the phagocytic cells that engulf them.
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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...
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[
Nature,
1996]
During the development of many, if not all, complex organisms, specific cells are marked out for elimination in a process known as programmed cell death, or apoptosis, a form of cell suicide. For example, during the development of the hermaphrodite nematode worm Caenorhabditis elegans, 131 of the 1,090 cells produced are genetically destined to die. Drosophila embryos without the necessary genes to execute this death programme do not survive. In vertebrates, failure to delete malformed or potentially autoreactive immune cells during development can eventually lead to autoimmunity or leukaemia. So too much or too little cell death threatens the whole organism.
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[
Nature,
2000]
We thought we knew what spectrin does. Is it not the elastic, membrane-bound protein that prevents red blood cells from rupturing as they circulate in the bloodstream? And does it not have the same supporting function in other cells? The second assumption has seldom been questioned over the past two decades, but has just been overturned by the power of experimental genetics, as described in three reports in the Journal of Cell Biology. The results may bear on human diseases such as muscular dystrophy.
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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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[
Discover,
1991]
Undulating under the microscope, its muscle and nerve cells visible within its transparent body, the tiny roundworm Caenorhabditis elegans is normally a creature of surprising grace. But one mutant strain is not elegans at all. It thrashes about in such an uncoordinated fashion that researchers have dubbed the mutant worm "unc"...
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[
Nature,
1988]
For myosin to function properly in muscle, its bipolar filaments must be assembled in ordered arrays. A major problem facing cell biologists is the control of local assembly of the filaments. Within non-muscle cells, the filaments are continually assembling and disassembling according to local signals. In muscle cells, however, myosin must be turning over continuously within a permanent array and, therefore, the cells must be replacing myosin subunits or whole filaments in an organized fashion. Two different approaches have now been applied to find out how this is achieved. The first is a classical genetic approach in which mutants of the nematode worm Caenorhabditis elegans with incorrect myosin assembly are isolated; and the second is by inducing expression of portions of the myosin molecule in bacteria. The differences in the information about myosin filament assembly provided by these two methods offer a nice contrast between genetic and molecular-biology approaches to a cell biology problem. Analysis of mutants reveals behaviours requiring molecular explanations, whereas the expression of pieces of the molecule gives information
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[
Nat Cell Biol,
2013]
Autophagy contributes to lipid catabolism through direct mobilization and breakdown of cellular lipid stores. Two recent studies reveal the regulatory mechanisms activated by cells during starvation to ensure that the cellular compartments involved in autophagic lipid catabolism are ready to receive, process and use these lipids. The regulators represent attractive therapeutic targets to help fight lipid-excess-associated diseases.
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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