The C. elegans is a is a free-living, transparent nematode, also called a round worm, about 1 mm in length. The C. elegant thrives in temperate soil environments.
This worm has been especially integral in science in the past decade. One reason is simply because of its short life span. In 2002, the Nobel Prize in Physiology or Medicine was awarded to Sydney Brenner, H. Robert Horvitz and John Sulston for their work on the genetics of organ development and programmed cell death in C. elegans. The 2006 Nobel Prize in Physiology or Medicine was awarded to Andrew Fire and Craig C. Mello for their discovery of RNA interference in C. elegans. The list is virtually bottomless. Most recently, not the least interesting, has been reported in the popular news journal, Plosbiology. (http://www.plosbiology.org/article/info%3Adoi%2F10.1371%2Fjournal.pbio.1001613) " Anthranilate Fluorescence Marks a Calcium-Propagated Necrotic Wave That Promotes Organismal Death in C. elegans."
"Oxidative and Thermal Stress Do Not Increase Blue Fluorescence. Lipofuscin is formed through accumulation of oxidatively damaged proteins and lipids. For example, raised oxygen level (40% O2) increases lipofuscin levels in human fibroblasts. To probe whether the blue fluorescent material in C. elegans gut granules is lipofuscin, we exposed them to normobaric hyperoxia (90% O2), and elevated iron levels. Both treatments significantly increased protein oxidative damage but neither increased blue fluorescence levels. Elevated expression of hsp-4::gfp is indicative of the unfolded protein response, symptomatic of protein damage. Heat shock increased hsp-4::gfp expression but not blue fluorescence. These results imply that C. elegans blue fluorescence is not generated by oxidative damage, suggesting that it is not lipofuscin. In this study, we have shown that conserved mechanisms underpinning neuronal necrosis can also contribute to organismal death. In so doing we provide the first insights into the last biological events in the life history of C. elegans: those leading to its final demise. Identification of an endogenous fluorescent marker of death led us to discover a calcium-generated wave of necrotic cell death that occurs during, and can contribute to, organismal death. We have also chemically defined the source of the endogenous blue fluorescence that is a salient characteristic of C. elegans. C. elegans Blue Fluorescence Is Not Lipofuscin. In this study we have defined a new phenomenon, death fluorescence, which may be useful in future as a marker of death in lifespan assays. While DF means that blue fluorescence cannot be used as a biomarker of aging we confirm that red fluorescence does increase with age. Moreover, tdo-2(RNAi) can be used to abrogate blue intestinal fluorescence to aid the viewing of expression of intestinally expressed fluorescent reporters. Materials and Methods Worm Maintenance and Strains Standard C. elegans strain maintenance and genetic manipulations were used. All strains were grown at 20°C on NGM plates seeded with E. coli OP50 as food source unless otherwise specified. N2 (Bristol) was the wild-type. Oxidative Stress Assays: Hyperoxia treatment. Young N2 adults were placed in either 90% O2 or air at 25°C for 5 d on 10 µM FUdR (fluorodeoxyuridine), OP50 seeded NGM plates. Iron treatment. Heat shock treatment. Carbonyl measurement. Blue fluorescence measurements. Microfluorimetry Time-lapse photography. Single-animal vermiculture. C. elegans Killing Assays and DF Measurements Worms were killed in three ways, all of which result in bursts of blue fluorescence of similar magnitude."
The C. elegans is important to the point that around the world many hundreds of scientists are working full time investigating its biology.
An international consortium of laboratories collaborated on a project to sequence the entire 100,000,000 bases of DNA found out that 40% of its genes have human matches.
It was the first worm to be sequenced. This worm is only 1 mm, but it is of gargantuan importance.
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