| Caenorhabditis elegans | |
|---|---|
 | |
| An adult hermaphroditeC. elegans worm | |
Scientific classification | |
| Kingdom: | Animalia |
| Phylum: | Nematoda |
| Class: | Chromadorea |
| Order: | Rhabditida |
| Family: | Rhabditidae |
| Genus: | Caenorhabditis |
| Species: | C. elegans |
| Binomial name | |
| Caenorhabditis elegans | |
| Subspecies | |
Caenorhabditis elegans (/ˌsiːnoʊræbˈdaɪtəsˈɛləɡæns/[6]) is a free-living transparentnematode about 1 mm in length that lives in temperate soil environments.[7] It is thetype species of its genus.[8] The name is ablend of the Greekcaeno- (recent),rhabditis (rod-like)[9] and Latinelegans (elegant). In 1900,Maupas initially named itRhabditides elegans.Osche placed it in thesubgenusCaenorhabditis in 1952, and in 1955,Dougherty raisedCaenorhabditis to the status ofgenus.[10]
C. elegans is an unsegmentedpseudocoelomate and lacks respiratory or circulatory systems.[11] Most of these nematodes arehermaphrodites and a few are males.[12] Males have specialised tails for mating that includespicules.
In 1963,Sydney Brenner proposed research intoC. elegans, primarily in the area of neuronal development. In 1974, he began research into themolecular anddevelopmental biology ofC. elegans, which has since been extensively used as amodel organism.[13] It was the firstmulticellular organism to have itswhole genome sequenced, and in 2019[14] it was the first organism to have itsconnectome (neuronal "wiring diagram") completed.[15][16][17]
As of 2024,[update] four Nobel prizes have been won for work done onC. elegans.[18]
C. elegans isunsegmented,vermiform, andbilaterally symmetrical. It has acuticle (a strong outer covering, as anexoskeleton), four mainepidermal cords, and a fluid-filledpseudocoelom (body cavity). It also has some of the same organ systems as larger animals. About one in a thousand individuals is male and the rest are hermaphrodites.[19] The basic anatomy ofC. elegans includes a mouth,pharynx,intestine,gonad, andcollagenous cuticle. Like all nematodes, they have neither a circulatory nor a respiratory system. The four bands of muscles that run the length of the body are connected to a neural system that allows the muscles to move the animal's body only as dorsal bending or ventral bending, but not left or right, except for the head, where the four muscle quadrants are wired independently from one another. When a wave of dorsal/ventral muscle contractions proceeds from the back to the front of the animal, the animal is propelled backwards. When a wave of contractions is initiated at the front and proceeds posteriorly along the body, the animal is propelled forwards. Because of this dorsal/ventral bias in body bends, any normal living, moving individual tends to lie on either its left side or its right side when observed crossing a horizontal surface. A set of ridges on the lateral sides of the body cuticle, the alae, is believed to give the animal added traction during these bending motions.
In relation to lipid metabolism,C. elegans does not have any specialized adipose tissues, apancreas, aliver, or even blood to deliver nutrients compared to mammals. Neutral lipids are instead stored in the intestine, epidermis, and embryos. Theepidermis corresponds to the mammalian adipocytes by being the maintriglyceride depot.[20]
The pharynx is a muscular food pump in the head ofC. elegans, which is triangular in cross-section. This grinds food and transports it directly to the intestine. A set of "valve cells" connects the pharynx to the intestine, but how this valve operates is not understood. After digestion, the contents of the intestine are released via the rectum, as is the case with all other nematodes.[21] No direct connection exists between the pharynx and theexcretory canal, which functions in the release of liquid urine.
Males have a single-lobed gonad, avas deferens, and a tail specialized for mating, which incorporatesspicules. Hermaphrodites have twoovaries,oviducts, andspermatheca, and a singleuterus.
There are 302 neurons inC. elegans, approximately one-third of all the somatic cells in the whole body.[22] Many neurons contain dendrites which extend from the cell to receive neurotransmitters or other signals, and aprocess that extends to the nerve ring (the "brain") for a synaptic connection with other neurons.[23]C. elegans has excitatorycholinergic and inhibitoryGABAergic motor neurons which connect with body wall muscles to regulate movement. In addition, these neurons and other neurons such as interneurons use a variety of neurotransmitters to control behaviors.[24]
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Numerous gut granules are present in the intestine ofC. elegans, the functions of which are still not fully known, as are many other aspects of this nematode, despite the many years that it has been studied. These gut granules are found in all of the Rhabditida orders. They are very similar tolysosomes in that they feature an acidic interior and the capacity forendocytosis, but they are considerably larger, reinforcing the view of their being storage organelles.A particular feature of the granules is that when they are observed underultraviolet light, they react by emitting an intense bluefluorescence. Another phenomenon seen is termed 'death fluorescence'. As the worms die, a dramatic burst of blue fluorescence is emitted. This death fluorescence typically takes place in an anterior to posterior wave that moves along the intestine, and is seen in both young and old worms, whether subjected to lethal injury or peacefully dying of old age.
Many theories have been posited on the functions of the gut granules, with earlier ones being eliminated by later findings. They are thought to store zinc as one of their functions. Recent chemical analysis has identified the blue fluorescent material they contain as aglycosylated form ofanthranilic acid (AA). The need for the large amounts of AA the many gut granules contain is questioned. One possibility is that the AA is antibacterial and used in defense against invading pathogens. Another possibility is that the granules provide photoprotection; the bursts of AA fluorescence entail the conversion of damaging UV light to relatively harmless visible light. This is seen as a possible link to themelanin–containingmelanosomes.[25]
The hermaphroditic worm is considered to be a specialized form of self-fertile female, as itssoma is female. The hermaphroditic germline produces malegametes first, and lays eggs through its uterus after internal fertilization. Hermaphrodites produce all theirsperm in the L4 stage (150 sperm cells per gonadal arm) and then produce onlyoocytes. The hermaphroditic gonad acts as an ovotestis with sperm cells being stored in the same area of the gonad as the oocytes until the first oocyte pushes the sperm into thespermatheca (a chamber wherein the oocytes become fertilized by the sperm).[26]
The male caninseminate the hermaphrodite, which will preferentially use male sperm (both types of sperm are stored in the spermatheca).
The sperm ofC. elegans is amoeboid, lackingflagella andacrosomes.[28] When self-inseminated, the wild-type worm lays about 300 eggs. When inseminated by a male, the number of progeny can exceed 1,000. Hermaphrodites do not typically mate with other hermaphrodites. At 20 °C, thelaboratory strain ofC. elegans (N2) has an average lifespan around 2–3 weeks and a generation time of 3 to 4 days.
C. elegans has five pairs ofautosomes and one pair ofsex chromosomes. Sex inC. elegans is based on anX0 sex-determination system. Hermaphrodites ofC. elegans have a matched pair of sex chromosomes (XX); the rare males have only one sex chromosome (X0).
C. elegans are mostly hermaphroditic organisms, producing both sperms andoocytes.[29] Males do occur in the population in a rate of approximately 1 in 200 hermaphrodites, but the two sexes are highly differentiated.[30][31] Males differ from their hermaphroditic counterparts in that they are smaller and can be identified through the shape of their tail.[31]C.elegans reproduce through a process calledandrodioecy. This means that they can reproduce in two ways: either through self-fertilization in hermaphrodites or through hermaphrodites breeding with males. Males are produced throughnon-disjunction of the X chromosomes during meiosis. The worms that reproduce through self-fertilization are at risk for highlinkage disequilibrium, which leads to lower genetic diversity in populations and an increase in accumulation ofdeleterious alleles.[32] InC. elegans, somatic sex determination is attributed to thetra-1 gene.[33] Thetra-1 is a gene within the TRA-1 transcription factor sex determination pathway that is regulated post-transcriptionally and works by promoting female development.[33] In hermaphrodites (XX), there are high levels oftra-1 activity, which produces the female reproductive system and inhibits male development.[29][33] At a certain time in their life cycle, one day before adulthood, hermaphrodites can be identified through the addition of a vulva near their tail. In males (XO), there are low levels oftra-1 activity, resulting in a male reproductive system.[33] Recent research has shown that there are three other genes,fem-1, fem-2, and fem-3, that negatively regulate the TRA-1 pathway and act as the final determiner of sex inC. elegans.[29]
The sex determination system inC. elegans is a topic that has been of interest to scientists for years.[30] Since they are used as a model organism, any information discovered about the way their sex determination system might have evolved could further the same evolutionary biology research in other organisms. After almost 30 years of research, scientists have begun to put together the pieces in the evolution of such a system.[30] What they have discovered is that there is a complex pathway involved that has several layers of regulation.[30] The closely related organismCaenorhabditis briggsae has been studied extensively and its whole genome sequence has helped put together the missing pieces in the evolution ofC. elegans sex determination.[30] It has been discovered that two genes have assimilated, leading to the proteins XOL-1 and MIX-1 having an effect on sex determination inC. elegans as well.[30] Mutations in the XOL-1 pathway leads to feminization inC. elegans .[34] Themix-1 gene is known to hypoactivate the X chromosome and regulates the morphology of the male tail inC. elegans.[35] Looking at the nematode as a whole, the male and hermaphrodite sex likely evolved from parallel evolution.[30] Parallel evolution is defined as similar traits evolving from an ancestor in similar conditions; simply put, the two species evolve in similar ways over time. An example of this would bemarsupial andplacental mammals. Scientists have also hypothesized that hermaphroditeasexual reproduction, or "selfing", could have evolved convergently by studying species similar toC. elegans[30] Other studies on the sex determination evolution suggest that genes involving sperm evolve at the faster rate than female genes.[36] However, sperm genes on the X chromosome have reduced evolution rates. Sperm genes have short coding sequences, high codon bias, and disproportionate representation amongorphan genes.[36] These characteristics of sperm genes may be the reason for their high rates of evolution and may also suggest how sperm genes evolved out of hermaphrodite worms. Overall, scientists have a general idea of the sex determination pathway inC. elegans, however, the evolution of how this pathway came to be is not yet well defined.
The fertilized zygote undergoes rotational holoblasticcleavage.
Sperm entry into the oocyte commences formation of an anterior-posterior axis.[37] The spermmicrotubule organizing center directs the movement of the spermpronucleus to the future posterior pole of the embryo, while also inciting the movement ofPAR proteins, a group of cytoplasmic determination factors, to their proper respective locations.[38] As a result of the difference in PAR protein distribution, the first cell division is highlyasymmetric.[39]C. elegansembryogenesis is among the best understood examples of asymmetric cell division.[40]
All cells of thegermline arise from a singleprimordial germ cell, called theP4 cell, established early inembryogenesis.[41][42] This primordial cell divides to generate two germline precursors that do not divide further until after hatching.[42]
The resulting daughter cells of the first cell division are called the AB cell (containing PAR-6 and PAR-3) and the P1 cell (containing PAR-1 and PAR-2). A second cell division produces the ABp and ABa cells from the AB cell, and the EMS and P2 cells from the P1 cell. This division establishes the dorsal-ventral axis, with the ABp cell forming the dorsal side and the EMS cell marking the ventral side.[43] ThroughWnt signaling, the P2 cell instructs the EMS cell to divide along the anterior-posterior axis.[44] ThroughNotch signaling, the P2 cell differentially specifies the ABp and ABa cells, which further defines the dorsal-ventral axis. The left-right axis also becomes apparent early in embryogenesis, although it is unclear exactly when specifically the axis is determined. However, most theories of the L-R axis development involve some kind of differences in cells derived from the AB cell.[45]
Gastrulation occurs after the embryo reaches the 24-cell stage.[46]C. elegans are a species ofprotostomes, so the blastopore eventually forms the mouth. Involution into the blastopore begins with movement of theendoderm cells and subsequent formation of the gut, followed by the P4 germline precursor, and finally themesoderm cells, including the cells that eventually form the pharynx. Gastrulation ends whenepiboly of the hypoblasts closes the blastopore.[47]
Under environmental conditions favourable forreproduction, hatchedlarvae develop through four larval stages - L1, L2, L3, and L4 - in just 3 days at 20 °C. When conditions are stressed, as in food insufficiency, excessive population density or high temperature,C. elegans can enter an alternative third larval stage, L2d, called thedauer stage (Dauer is German for permanent). A specific dauer pheromone regulates entry into the dauer state. This pheromone is composed of similar derivatives of the 3,6-dideoxy sugar,ascarylose. Ascarosides, named after the ascarylose base, are involved in many sex-specific and social behaviors.[48] In this way, they constitute a chemical language thatC. elegans uses to modulate various phenotypes. Dauer larvae are stress-resistant; they are thin and their mouths are sealed with a characteristic dauer cuticle and cannot take in food. They can remain in this stage for a few months.[49][50] The stage ends when conditions improve favour further growth of the larva, now moulting into the L4 stage, even though the gonad development is arrested at the L2 stage.[51]
Each stage transition is punctuated by a molt of the worm's transparent cuticle. Transitions through these stages are controlled by genes of the heterochronic pathway, an evolutionarily conserved set of regulatory factors.[52] Many heterochronic genes code formicroRNAs, which repress the expression of heterochronictranscription factors and other heterochronic miRNAs.[53] miRNAs were originally discovered inC. elegans.[54] Important developmental events controlled by heterochronic genes include the division and eventualsyncitial fusion of the hypodermic seam cells, and their subsequent secretion of the alae in young adults. It is believed that the heterochronic pathway represents an evolutionarily conserved predecessor tocircadian clocks.[55]
Some nematodes have a fixed, genetically determined number of cells, a phenomenon known aseutely. The adultC. elegans hermaphrodite has 959 somatic cells and the male has 1033 cells,[56][57][58] although it has been suggested that the number of their intestinal cells can increase by one to three in response to gut microbes experienced by mothers.[59] Much of the literature describes the cell number in males as 1031, but the discovery of a pair of left and right MCM neurons increased the number by two in 2015.[58] The number of cells does not change after cell division ceases at the end of the larval period, and subsequent growth is due solely to an increase in the size of individual cells.[60]
The differentCaenorhabditis species occupy various nutrient- and bacteria-rich environments. They feed on the bacteria that develop in decaying organic matter (microbivory). They possess chemosensory receptors which enable the detection of bacteria and bacterial-secreted metabolites (such as iron siderophores), so that they can migrate towards their bacterial prey.[61] Soil lacks enough organic matter to support self-sustaining populations.C. elegans can survive on a diet of a variety of bacteria, but its wild ecology is largely unknown. Most laboratory strains were taken from artificial environments such as gardens andcompost piles. More recently,C. elegans has been found to thrive in other kinds of organic matter, particularly rotting fruit.[62]C. elegans can also ingest pollutants, especially tinynanoplastics, which could enable the association with antibiotic-resistant bacteria, resulting in the dissemination of nanoplastics and antibiotic-resistant bacteria byC. elegans across the soil.[63] Moreover,microplastics can alter the bacterial food preference byC. elegans over generations, resulting inC. elegans preferring microplastic-contaminated food over non-contaminated bacteria.[64]
C. elegans can also use different species ofyeast, includingCryptococcus laurentii andC. kuetzingii, as sole sources of food.[65] Although abacterivore,C. elegans can be killed by a number of pathogenic bacteria, including human pathogens such asStaphylococcus aureus,[66]Pseudomonas aeruginosa,[67]Salmonella enterica orEnterococcus faecalis.[68] Pathogenic bacteria can also form biofilms, whose sticky exopolymer matrix could impedeC. elegans motility[69] and cloaks bacterial quorum sensing chemoattractants from predator detection.[70]
Invertebrates such asmillipedes,insects,isopods, andgastropods can transport dauer larvae to various suitable locations. The larvae have also been seen to feed on their hosts when they die.[71]
Nematodes can survivedesiccation, and inC. elegans, the mechanism for this capability has been demonstrated to belate embryogenesis abundant proteins.[72]
C. elegans, as other nematodes, can be eaten by predator nematodes and other omnivores, including some insects.[73]
TheOrsay virus is a virus that affectsC. elegans, as well as theCaenorhabditis elegans Cer1 virus[74] and theCaenorhabditis elegans Cer13 virus.
Wild isolates ofCaenorhabditis elegans are regularly found with infections byMicrosporidia fungi. One such species,Nematocida parisii, replicates in the intestines ofC. elegans.[75]
Arthrobotrys oligospora is themodel organism for interactions between fungi and nematodes.[76] It is the most common and widespread nematode capturing fungus.
In 1963,Sydney Brenner proposed usingC. elegans as amodel organism for the investigation primarily of neural development in animals. It is one of the simplest organisms with anervous system. The neurons do not fireaction potentials, and do not express anyvoltage-gated sodium channels.[77] In the hermaphrodite, this system comprises 302neurons[78] the pattern of which has been comprehensively mapped,[14] in what is known as aconnectome,[79] and shown to be asmall-world network.[80]
Research has explored the neural and molecular mechanisms that control several behaviors ofC. elegans, includingchemotaxis,thermotaxis,mechanotransduction,learning,memory, andmating behaviour.[81] In 2019 the connectome of the male was published using a technique distinct from that used for the hermaphrodite. The same paper used the new technique to redo the hermaphrodite connectome, finding 1,500 new synapses.[82]
It has been used as a model organism to study molecular mechanisms in metabolic diseases.[83] Brenner also chose it as it is easy to grow in bulk populations, and convenient for genetic analysis.[84] It is amulticellulareukaryotic organism, yet simple enough to be studied in great detail. The transparency ofC. elegans facilitates the study ofcellular differentiation and other developmental processes in the intact organism. The spicules in the male clearly distinguish males from females.Strains are cheap to breed and can be frozen. When subsequently thawed, they remain viable, allowing long-term storage.[13] Maintenance is easy when compared to other multicellular model organisms. A few hundred nematodes can be kept on a singleagar plate and suitable growth medium. Brenner described the use of a mutant ofE. coli – OP50. OP50 is auracil-requiring organism and its deficiency in the plate prevents the overgrowth of bacteria which would obscure the worms.[85] The use of OP50 does not demand any major laboratory safety measures, since it is non-pathogenic and easily grown in Luria-Bertani (LB) media overnight.[86]
The developmental fate of every singlesomatic cell (959 in the adult hermaphrodite; 1031 in the adult male) has been mapped.[87][88] These patterns of cell lineage are largely invariant between individuals, whereas in mammals, cell development is more dependent on cellular cues from the embryo.
As mentioned previously, the first cell divisions of earlyembryogenesis inC. elegans are among the best understood examples ofasymmetric cell divisions, and the worm is a very popular model system for studying developmental biology.[40]
Programmed cell death (apoptosis) eliminates many additional cells (131 in the hermaphrodite, most of which would otherwise becomeneurons); this "apoptotic predictability" has contributed to the elucidation of someapoptotic genes. Cell death-promoting genes and a single cell-death inhibitor have been identified.[89]
RNA interference (RNAi) is a relatively straightforward method of disrupting the function of specific genes.Silencing the function of a gene can sometimes allow a researcher to infer its possible function. The nematode can be soaked in, injected with,[90] or fed with geneticallytransformed bacteria thatexpress the double-stranded RNA of interest, the sequence of which complements the sequence of the gene that the researcher wishes to disable.[91]RNAi has emerged as a powerful tool in the study of functional genomics.C. elegans has been used to analyse gene functions and claim the promise of future findings in the systematic genetic interactions.[92]
Environmental RNAi uptake is much worse in other species of worms in the genusCaenorhabditis. Although injecting RNA into the body cavity of the animal inducesgene silencing in most species, onlyC. elegans and a few other distantly related nematodes can take up RNA from the bacteria they eat for RNAi.[93] This ability has been mapped down to a single gene,sid-2, which, when inserted as atransgene in other species, allows them to take up RNA for RNAi asC. elegans does.[94]
Research intomeiosis has been considerably simplified since every germ cell nucleus is at the same given position as it moves down the gonad, so is at the same stage in meiosis. In an early phase of meiosis, the oocytes become extremely resistant to radiation and this resistance depends on expression of genesrad51 andatm that have key roles in recombinational repair.[95][96] Genemre-11 also plays a crucial role in recombinational repair of DNA damage during meiosis.[97] Furthermore, duringmeiosis inC. elegans the tumor suppressorBRCA1/BRC-1 and the structural maintenance of chromosomesSMC5/SMC6 protein complex interact to promote high fidelity repair ofDNA double-strand breaks.[98]
A study of the frequency of outcrossing in natural populations showed thatselfing is the predominant mode of reproduction inC. elegans, but that infrequent outcrossing events occur at a rate around 1%.[99] Meioses that result in selfing are unlikely to contribute significantly to beneficial genetic variability, but these meioses may provide the adaptive benefit of recombinational repair of DNA damages that arise, especially under stressful conditions.[100]
Nicotinedependence can also be studied usingC. elegans because it exhibits behavioral responses to nicotine that parallel those of mammals. These responses include acute response, tolerance, withdrawal, and sensitization.[101]
As for most model organisms, scientists that work in the field curate a dedicated online database andWormBase is that forC. elegans. The WormBase attempts to collate all published information onC. elegans and other related nematodes. Information onC. elegans is included with data on other model organisms in the Alliance of Genome Resources.[102]
C. elegans has been a model organism for research intoageing; for example, the inhibition of aninsulin-like growth factor signaling pathway has been shown to increase adult lifespan threefold;[103][104] while glucose feeding promotes oxidative stress and reduces adult lifespan by a half.[83] Similarly, induced degradation of an insulin/IGF-1 receptor late in life extended life expectancy of worms dramatically.[105] Long-livedmutants ofC. elegans were demonstrated to be resistant tooxidative stress andUV light.[106] These long-lived mutants had a higherDNA repair capability than wild-typeC. elegans.[106] Knockdown of thenucleotide excision repair gene Xpa-1 increased sensitivity to UV and reduced thelife span of the long-lived mutants. These findings indicate thatDNA repair capability underlies longevity. Consistent with the idea that oxidative DNA damage causes aging, it was found that inC. elegans,exosome-mediated delivery ofsuperoxide dismutase (SOD) reduces the level ofreactive oxygen species (ROS) and significantly extends lifespan, i.e. delays aging under normal, as well as hostile conditions.[107]
The capacity to repair DNA damage by the process of nucleotide excision repair declines with age.[108]
C. elegans exposed to 5mMlithium chloride (LiCl) showed lengthened life spans.[109] When exposed to 10μM LiCl, reduced mortality was observed, but not with 1μM.[110]
C. elegans has been instrumental in the identification of the functions of genes implicated inAlzheimer's disease, such aspresenilin.[111] Moreover, extensive research onC. elegans has identifiedRNA-binding proteins as essential factors during germline and early embryonic development.[112]
Telomeres, the length of which have been shown to correlate with increased lifespan and delayed onset ofsenescence in a multitude of organisms, fromC. elegans[113][114] to humans,[115] show an interesting behaviour inC. elegans. WhileC. elegans maintains its telomeres in a canonical way similar to other eukaryotes, in contrastDrosophila melanogaster is noteworthy in its use ofretrotransposons to maintain its telomeres,[116] duringknock-out of thecatalytic subunit of the telomerase (trt-1)C. elegans can gain the ability of alternative telomere lengthening (ALT).C. elegans was the first eukaryote to gain ALT functionality after knock-out of the canonicaltelomerase pathway.[117] ALT is also observed in about 10-15% of all clinical cancers.[118] ThusC. elegans is a prime candidate for ALT research.[119][120][121] Bayat et al. showed the paradoxical shortening of telomeres duringtrt-1over-expression which lead to nearsterility while the worms even exhibited a slight increase in lifespan, despite shortened telomeres.[122]
C. elegans is notable inanimal sleep studies as the most primitive organism to display sleep-like states. InC. elegans, alethargus phase occurs shortly before eachmoult.[123]C. elegans has also been demonstrated to sleep after exposure to physical stress, including heat shock, UV radiation, and bacterial toxins.[124]
While the worm has no eyes, it has been found to be sensitive to light due to a third type of light-sensitive animalphotoreceptor protein,LITE-1, which is 10 to 100 times more efficient at absorbing light than the other two types of photopigments (opsins andcryptochromes) found in the animal kingdom.[125]
C. elegans is remarkably adept at tolerating acceleration. It can withstand 400,000g's, according to geneticists at the University of São Paulo in Brazil. In an experiment, 96% of them were still alive without adverse effects after an hour in an ultracentrifuge.[126]
Having a small size and short life cycle, C. elegans is one of the few organisms that can enable in vivohigh throughput screening (HTS) platforms for the evaluation of chemical libraries of drugs and toxins in a multicellular organism.[127] Orthologous phenotypes observable in C. elegans for human diseases have the potential to enable profiling of drug library profiling that can inform potential repurposing of existing approved drugs for therapeutic indications in humans.[128]
C. elegans made news when specimens were discovered to have survived theSpace ShuttleColumbia disaster in February 2003.[129] Later, in January 2009, live samples ofC. elegans from theUniversity of Nottingham were announced to be spending two weeks on theInternational Space Station that October, in aspace research project to explore the effects ofzero gravity on muscle development and physiology. The research was primarily about genetic basis ofmuscle atrophy, which relates tospaceflight or being bed-ridden,geriatric, ordiabetic.[130] Descendants of the worms aboard Columbia in 2003 were launched into space onEndeavour for theSTS-134 mission.[131] Additional experiments on muscle dystrophy during spaceflight were carried on board the ISS starting in 2018.[132] It was shown that the genes affecting muscles attachment were expressed less in space. However, it has yet to be seen if this affects muscle strength.
 Karyotype ofC. elegans explanation of colors Mitotic chromosomes ofC. elegans. DNA (red)/Kinetochores (green).Holocentric organisms, includingC. elegans, assemble diffuse kinetochores along the entire poleward face of each sister chromatid. | |
| NCBI ID | GCA_000002985.3 |
|---|---|
| Ploidy | diploid |
| Genome size | 101.169 Mb (haploid) |
| Number ofchromosomes | 5 pairs of autosomes (I, II, III, IV and V) + 1 or 2 sex chromosomes (X[133]) |
| Year of completion | 1998 |
| Sequencedorganelle | mitochondrion |
| Organelle size | 0,01 Mb |
| UCSC Genome Browser assembly ID | ce11 |
C. elegans was the first multicellular organism to have itswhole genome sequenced. The sequence was published in 1998,[134] although some small gaps were present; the last gap was finished by October 2002.[citation needed] In the run up to the whole genome theC. elegans Sequencing Consortium/C. elegans Genome Project released several partial scans including Wilson et al. 1994.[135][136][137]
TheC. elegans genome is about 100 millionbase pairs long and consists of six pairs of chromosomes in hermaphrodites or five pairs of autosomes with XO chromosome in maleC. elegans and amitochondrial genome. Itsgene density is about one gene per fivekilo-base pairs.Introns make up 26% andintergenic regions 47% of the genome. Many genes are arranged in clusters and how many of these areoperons is unclear.[138]C. elegans and other nematodes are among the few eukaryotes currently known to have operons; these includetrypanosomes,flatworms (notably thetrematodeSchistosoma mansoni), and a primitivechordatetunicateOikopleura dioica. Many more organisms are likely to be shown to have these operons.[139]
The genome contains an estimated 20,470protein-codinggenes.[140] About 35% ofC. elegans genes have humanhomologs. Remarkably, human genes have been shown repeatedly to replace theirC. elegans homologs when introduced intoC. elegans. Conversely, manyC. elegans genes can function similarly to mammalian genes.[49]
The number of knownRNA genes in the genome has increased greatly due to the 2006 discovery of a new class called21U-RNA genes,[141] and the genome is now believed to contain more than 16,000 RNA genes, up from as few as 1,300 in 2005.[142]
Scientific curators continue to appraise the set of known genes; new gene models continue to be added and incorrect ones modified or removed.
The referenceC. elegans genome sequence continues to change as new evidence reveals errors in the original sequencing. Most changes are minor, adding or removing only a few base pairs of DNA. For example, the WS202 release of WormBase (April 2009) added two base pairs to the genome sequence.[143] Sometimes, more extensive changes are made as noted in the WS197 release of December 2008, which added a region of over 4,300 bp to the sequence.[144][145]
TheC. elegans Genome Project's Wilson et al. 1994 foundCelVav[137] and avon Willebrand factor A domain[135] and with Wilson et al. 1998 provides the first credible evidence for anaryl hydrocarbon receptor (AHR)homolog outside of vertebrates.[136] 2
In 2003, the genome sequence of the related nematodeC. briggsae was also determined, allowing researchers to study thecomparative genomics of these two organisms.[146] The genome sequences of more nematodes from the samegenus e.g.,C. remanei,[147]C. japonica[148] andC. brenneri (named after Brenner), have also been studied using theshotgun sequencing technique.[149] These sequences have now been completed.[150][151]
As of 2014,C. elegans is the most basal species in the 'Elegans' group (10 species) of the 'Elegans' supergroup (17 species) in phylogenetic studies. It forms a branch of its own distinct to any other species of the group.[152]
Tc1 transposon is a DNA transposon active inC. elegans.
Several scientists have won theNobel Prize in Physiology or Medicine for scientific discoveries made working withC. elegans. It was awarded in 2002 toSydney Brenner,H. Robert Horvitz, andJohn Sulston for their work on the genetics of organ development andprogrammed cell death, in 2006 toAndrew Fire andCraig C. Mello for their discovery ofRNA interference, and in 2024 toVictor Ambros andGary Ruvkun for their discovery ofmicroRNA and its role in gene regulation.[153][154]In 2008,Martin Chalfie shared aNobel Prize in Chemistry for his work ongreen fluorescent protein; some of the research involved the use ofC. elegans.
Many scientists who researchC. elegansclosely connect to Sydney Brenner, with whom almost all research in this field began in the 1970s; they have worked as either apostdoctoral or apostgraduate researcher in Brenner's lab or in the lab of someone who previously worked with Brenner. Most who worked in his lab later established their own worm research labs, thereby creating a fairly well-documented "lineage" ofC. elegans scientists, which was recorded into theWormBase database in some detail at the 2003 International Worm Meeting.[155]
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