Editing Caenorhabditis elegans (section)

== Use as a model organism ==
{{Further|History of research on Caenorhabditis elegans}}
[[File:Epigenetic-Regulation-of-Histone-H3-Serine-10-Phosphorylation-Status-by-HCF-1-Proteins-in-C.-pone.0001213.s003.ogv|thumb|Asymmetric cell divisions during early embryogenesis of wild-type ''C. elegans'']]
In 1963, [[Sydney Brenner]] proposed using ''C. elegans'' as a [[model organism]] for the investigation primarily of neural development in animals. It is one of the simplest organisms with a [[nervous system]]. The neurons do not fire [[action potentials]], and do not express any [[voltage-gated sodium channel]]s.<ref>{{cite journal | vauthors = Clare JJ, Tate SN, Nobbs M, Romanos MA | title = Voltage-gated sodium channels as therapeutic targets | journal = Drug Discovery Today | volume = 5 | issue = 11 | pages = 506–520 | date = November 2000 | pmid = 11084387 | doi = 10.1016/S1359-6446(00)01570-1 }}</ref> In the hermaphrodite, this system comprises 302 [[neuron]]s<ref>{{cite journal |bibcode=2007AcPPB..38.2201K |title=Dynamics of the Model of the Caenorhabditis Elegans Neural Network |journal=Acta Physica Polonica B |volume=38 |issue=6 |pages=2201 | vauthors = Kosinski RA, Zaremba M  |year=2007 }}</ref> the pattern of which has been comprehensively mapped,<ref name="da freakin nectome">
{{cite journal
 |title=Whole-animal connectomes of both ''Caenorhabditis elegans'' sexes
 |last1=Cook
 |first1=SJ
 |last2=Jarrell
 |first2=TA
 |last3=Brittin
 |first3=CA
 |last4=Wang
 |first4=Y
 |last5=Bloniarz
 |first5=AE
 |last6=Yakovlev
 |first6=MA
 |last7=Nguyen
 |first7=KCQ
 |last8=Tang
 |first8=Lt-H
 |last9=Bayer
 |first9=EA
 |last10=Duerr
 |first10=JS
 |last11=Bulow
 |first11=HE
 |last12=Hobert
 |first12=O
 |last13=Hall
 |first13=DH
 |last14=Emmons
 |first14=SW
 |journal=Nature
 |date=3 December 2019
 |volume=571
 |issue=7763
 |pages=63–71
 |publisher= US National Library of Medicine, National Institutes of Health 
 |doi=10.1038/s41586-019-1352-7
 |pmc=6889226
 |pmid=31270481
|bibcode=2019Natur.571...63C
 }}</ref> in what is known as a [[connectome]],<ref name="Brouillette">{{cite journal |last1=Brouillette |first1=Monique |title=Mapping the brain to understand the mind |journal=Knowable Magazine |date=21 April 2022 |doi=10.1146/knowable-042122-1|doi-access=free |url=https://knowablemagazine.org/article/mind/2022/mapping-brain-understand-mind |language=en}}</ref> and shown to be a [[small-world network]].<ref>{{cite journal | vauthors = Watts DJ, Strogatz SH | title = Collective dynamics of 'small-world' networks | journal = Nature | volume = 393 | issue = 6684 | pages = 440–2 | date = June 1998 | pmid = 9623998 | doi = 10.1038/30918 | bibcode = 1998Natur.393..440W | s2cid = 4429113 }}</ref>

Research has explored the neural and molecular mechanisms that control several behaviors of ''C. elegans'', including [[chemotaxis]], [[thermotaxis]], [[mechanotransduction]], [[learning]], [[memory]], and [[mating]] behaviour.<ref>{{cite journal | vauthors = Schafer WR | title = Deciphering the neural and molecular mechanisms of C. elegans behavior | journal = Current Biology | volume = 15 | issue = 17 | pages = R723–9 | date = September 2005 | pmid = 16139205 | doi = 10.1016/j.cub.2005.08.020 | author-link1 = William Schafer (neuroscientist) | doi-access = free | bibcode = 2005CBio...15.R723S }}</ref> 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.<ref>{{cite journal | vauthors = Cook SJ, Jarrell TA, Brittin CA, Wang Y, Bloniarz AE, Yakovlev MA, Nguyen KC, Tang LT, Bayer EA, Duerr JS, Bülow HE, Hobert O, Hall DH, Emmons SW | display-authors = 6 | title = Whole-animal connectomes of both Caenorhabditis elegans sexes | journal = Nature | volume = 571 | issue = 7763 | pages = 63–71 | date = July 2019 | pmid = 31270481 | pmc = 6889226 | doi = 10.1038/s41586-019-1352-7 | bibcode = 2019Natur.571...63C }}</ref>

It has been used as a model organism to study molecular mechanisms in metabolic diseases.<ref name="ReferenceC">{{cite journal | vauthors = Alcántar-Fernández J, Navarro RE, Salazar-Martínez AM, Pérez-Andrade ME, Miranda-Ríos J | title = Caenorhabditis elegans respond to high-glucose diets through a network of stress-responsive transcription factors | journal = PLOS ONE | volume = 13 | issue = 7 | pages = e0199888 | date = 2018 | pmid = 29990370 | pmc = 6039004 | doi = 10.1371/journal.pone.0199888 | bibcode = 2018PLoSO..1399888A | doi-access = free }}</ref> 
Brenner also chose it as it is easy to grow in bulk populations, and convenient for genetic analysis.<ref>{{cite web |last=Avery |first=L |title=Sydney Brenner |url=http://elegans.swmed.edu/Sydney.html |publisher=[[Southwestern Medical Center]] |url-status=dead |archive-url=https://web.archive.org/web/20110815143145/http://elegans.swmed.edu/Sydney.html |archive-date=August 15, 2011 }} [http://elegans.som.vcu.edu/Sydney.html Alt. URL] {{Webarchive|url=https://web.archive.org/web/20131208060434/http://elegans.som.vcu.edu/Sydney.html |date=2013-12-08 }}</ref> It is a [[multicellular]] [[Eukaryote|eukaryotic]] organism, yet simple enough to be studied in great detail. The transparency of ''C. elegans'' facilitates the study of [[cellular differentiation]] and other developmental processes in the intact organism. The spicules in the male clearly distinguish males from females. [[Strain (biology)|Strains]] are cheap to breed and can be frozen. When subsequently thawed, they remain viable, allowing long-term storage.<ref name="ReferenceB"/> Maintenance is easy when compared to other multicellular model organisms. A few hundred nematodes can be kept on a single [[agar plate]] and suitable growth medium. Brenner described the use of a mutant of ''E. coli'' – OP50. OP50 is a [[uracil]]-requiring organism and its deficiency in the plate prevents the overgrowth of bacteria which would obscure the worms.<ref>{{cite journal | last1 = Brenner | first1 = S | year = 1974 | title = The genetics of Caenorhabditis elegans. | journal = Genetics | volume = 77 | issue = 1| pages = 71–94 | doi = 10.1093/genetics/77.1.71 | pmc = 1213120 | pmid = 4366476 }}</ref> 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.<ref>{{Cite web|url=http://www.wormbook.org/chapters/www_behavior/behavior.html#sec1|title=Behavior|website=www.wormbook.org|access-date=2018-09-26}}</ref>

=== Cell lineage mapping ===
The developmental fate of every single [[somatic cell]] (959 in the adult hermaphrodite; 1031 in the adult male) has been mapped.<ref>
{{cite journal | vauthors = Sulston JE, Horvitz HR | title = Post-embryonic cell lineages of the nematode, Caenorhabditis elegans | journal = Developmental Biology | volume = 56 | issue = 1 | pages = 110–56 | date = March 1977 | pmid = 838129 | doi = 10.1016/0012-1606(77)90158-0 }}</ref><ref>
{{cite journal | vauthors = Kimble J, Hirsh D | title = The postembryonic cell lineages of the hermaphrodite and male gonads in Caenorhabditis elegans | journal = Developmental Biology | volume = 70 | issue = 2 | pages = 396–417 | date = June 1979 | pmid = 478167 | doi = 10.1016/0012-1606(79)90035-6 }}</ref> 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 early [[embryogenesis]] in ''C. elegans'' are among the best understood examples of [[asymmetric cell division]]s, and the worm is a very popular model system for studying developmental biology.<ref name="ReferenceA"/>

=== Programmed cell death ===
Programmed cell death ([[apoptosis]]) eliminates many additional cells (131 in the hermaphrodite, most of which would otherwise become [[neuron]]s); this "apoptotic predictability" has contributed to the elucidation of some [[Caretaker gene|apoptotic genes]]. Cell death-promoting genes and a single cell-death inhibitor have been identified.<ref>{{cite journal | vauthors = Peden E, Killian DJ, Xue D | title = Cell death specification in C. elegans | journal = Cell Cycle | volume = 7 | issue = 16 | pages = 2479–84 | date = August 2008 | pmid = 18719375 | pmc = 2651394 | doi = 10.4161/cc.7.16.6479 }}</ref>

=== RNA interference and gene silencing ===
[[File:C elegans stained.jpg|thumb|right|Wild-type ''C. elegans'' hermaphrodite stained with the fluorescent dye [[Texas Red]] to highlight the nuclei of all cells]]

[[RNA interference]] (RNAi) is a relatively straightforward method of disrupting the function of specific genes. [[Gene silencing|Silencing]] the function of a gene can sometimes allow a researcher to infer its possible function. The nematode can be soaked in, injected with,<ref>{{Cite web|url=https://www.youtube.com/watch?v=Wam-kw4xwZc| archive-url=https://ghostarchive.org/varchive/youtube/20211117/Wam-kw4xwZc| archive-date=2021-11-17 | url-status=live|title=Injection of C. elegans Gonads|last=NIDDK|first=National Institute of Diabetes and Digestive and Kidney Diseases|website=YouTube|date=March 5, 2015|access-date=March 21, 2020}}{{cbignore}}</ref> or fed with genetically [[Transformation (genetics)|transformed]] bacteria that [[gene expression|express]] the double-stranded RNA of interest, the sequence of which complements the sequence of the gene that the researcher wishes to disable.<ref>
{{cite journal | vauthors = Kamath RS, Fraser AG, Dong Y, Poulin G, Durbin R, Gotta M, Kanapin A, Le Bot N, Moreno S, Sohrmann M, Welchman DP, Zipperlen P, Ahringer J | title = Systematic functional analysis of the Caenorhabditis elegans genome using RNAi | journal = Nature | volume = 421 | issue = 6920 | pages = 231–7 | date = January 2003 | pmid = 12529635 | doi = 10.1038/nature01278 | bibcode = 2003Natur.421..231K | hdl = 10261/63159 | s2cid = 15745225 }}</ref>
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.<ref>{{cite journal | vauthors = Fortunato A, Fraser AG | title = Uncover genetic interactions in Caenorhabditis elegans by RNA interference | journal = Bioscience Reports | volume = 25 | issue = 5–6 | pages = 299–307 | date = 2005 | pmid = 16307378 | doi = 10.1007/s10540-005-2892-7 | s2cid = 6983519  }}</ref>

Environmental RNAi uptake is much worse in other species of worms in the genus ''Caenorhabditis''. Although injecting RNA into the body cavity of the animal induces [[gene silencing]] in most species, only ''C. elegans'' and a few other distantly related nematodes can take up RNA from the bacteria they eat for RNAi.<ref>
{{cite journal | vauthors = Félix MA | title = RNA interference in nematodes and the chance that favored Sydney Brenner | journal = Journal of Biology | volume = 7 | issue = 9 | pages = 34 | date = November 2008 | pmid = 19014674 | pmc = 2776389 | doi = 10.1186/jbiol97 | doi-access = free }}</ref> This ability has been mapped down to a single gene, ''sid-2'', which, when inserted as a [[transgene]] in other species, allows them to take up RNA for RNAi as ''C. elegans'' does.<ref>
{{cite journal | vauthors = Winston WM, Sutherlin M, Wright AJ, Feinberg EH, Hunter CP | title = Caenorhabditis elegans SID-2 is required for environmental RNA interference | journal = Proceedings of the National Academy of Sciences of the United States of America | volume = 104 | issue = 25 | pages = 10565–70 | date = June 2007 | pmid = 17563372 | pmc = 1965553 | doi = 10.1073/pnas.0611282104 | bibcode = 2007PNAS..10410565W | doi-access = free }}</ref>

=== Cell division and cell cycle ===
Research into [[meiosis]] 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 genes ''rad51'' and ''atm'' that have key roles in recombinational repair.<ref name="pmid11058122">{{cite journal | vauthors = Takanami T, Mori A, Takahashi H, Higashitani A | title = Hyper-resistance of meiotic cells to radiation due to a strong expression of a single recA-like gene in Caenorhabditis elegans | journal = Nucleic Acids Research | volume = 28 | issue = 21 | pages = 4232–6 | date = November 2000 | pmid = 11058122 | pmc = 113154 | doi = 10.1093/nar/28.21.4232 }}</ref><ref name="pmid14646232">{{cite journal | vauthors = Takanami T, Zhang Y, Aoki H, Abe T, Yoshida S, Takahashi H, Horiuchi S, Higashitani A | title = Efficient repair of DNA damage induced by heavy ion particles in meiotic prophase I nuclei of Caenorhabditis elegans | journal = Journal of Radiation Research | volume = 44 | issue = 3 | pages = 271–6 | date = September 2003 | pmid = 14646232 | doi = 10.1269/jrr.44.271 | bibcode = 2003JRadR..44..271T | doi-access = free }}</ref> Gene ''[[MRE11A|mre-11]]'' also plays a crucial role in recombinational repair of DNA damage during meiosis.<ref name=Chin>{{cite journal | vauthors = Chin GM, Villeneuve AM | title = C. elegans mre-11 is required for meiotic recombination and DNA repair but is dispensable for the meiotic G(2) DNA damage checkpoint | journal = Genes & Development | volume = 15 | issue = 5 | pages = 522–34 | date = March 2001 | pmid = 11238374 | pmc = 312651 | doi = 10.1101/gad.864101 }}</ref>  Furthermore, during [[meiosis]] in ''C. elegans'' the tumor suppressor [[BRCA1]]/BRC-1 and the structural maintenance of chromosomes [[SMC5]]/[[SMC6]] protein complex interact to promote high fidelity repair of [[Double-strand break repair model|DNA double-strand breaks]].<ref>{{cite journal |vauthors=Toraason E, Salagean A, Almanzar DE, Brown JE, Richter CM, Kurhanewicz NA, Rog O, Libuda DE |title=BRCA1/BRC-1 and SMC-5/6 regulate DNA repair pathway engagement during Caenorhabditis elegans meiosis |journal=eLife |volume=13 |issue= |pages= |date=August 2024 |pmid=39115289 |pmc=11368404 |doi=10.7554/eLife.80687 |doi-access=free |url=}}</ref>

A study of the frequency of outcrossing in natural populations showed that [[selfing]] is the predominant mode of reproduction in ''C. elegans'', but that infrequent outcrossing events occur at a rate around 1%.<ref name="pmid16005289">{{cite journal | vauthors = Barrière A, Félix MA | title = High local genetic diversity and low outcrossing rate in Caenorhabditis elegans natural populations | journal = Current Biology | volume = 15 | issue = 13 | pages = 1176–84 | date = July 2005 | pmid = 16005289 | doi = 10.1016/j.cub.2005.06.022 | arxiv = q-bio/0508003 | bibcode = 2005CBio...15.1176B | s2cid = 2229622 }}</ref>  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.<ref>Bernstein H, Bernstein C (July 2010) "Evolutionary Origin of Recombination during Meiosis," BioScience 60(7), 498-505. https://doi.org/10.1525/bio.2010.60.7.5</ref>

=== Drug abuse and addiction ===
[[Nicotine]] [[substance dependence|dependence]] can also be studied using ''C. elegans'' because it exhibits behavioral responses to nicotine that parallel those of mammals. These responses include acute response, tolerance, withdrawal, and sensitization.<ref>{{cite journal | vauthors = Feng Z, Li W, Ward A, Piggott BJ, Larkspur ER, Sternberg PW, Xu XZ | title = A C. elegans model of nicotine-dependent behavior: regulation by TRP-family channels | journal = Cell | volume = 127 | issue = 3 | pages = 621–33 | date = November 2006 | pmid = 17081982 | pmc = 2859215 | doi = 10.1016/j.cell.2006.09.035 }}</ref>

=== Biological databases ===
As for most model organisms, scientists that work in the field curate a dedicated online database and [[WormBase]] is that for ''C. elegans''. The WormBase attempts to collate all published information on ''C. elegans'' and other related nematodes. Information on ''C. elegans'' is included with data on other model organisms in the Alliance of Genome Resources.<ref>{{Cite web |title=Alliance of Genome Resources Community Forum |url=https://community.alliancegenome.org/ |access-date=2024-08-01 |website=Alliance of Genome Resources Community Forum |language=en}}</ref>

=== Ageing ===
''C. elegans'' has been a model organism for research into [[ageing]]; for example, the inhibition of an [[insulin-like growth factor]] signaling pathway has been shown to increase adult lifespan threefold;<ref>{{cite journal | vauthors = Wolkow CA, Kimura KD, Lee MS, Ruvkun G | title = Regulation of C. elegans life-span by insulinlike signaling in the nervous system | journal = Science | volume = 290 | issue = 5489 | pages = 147–50 | date = October 2000 | pmid = 11021802 | doi = 10.1126/science.290.5489.147 | bibcode = 2000Sci...290..147W }}</ref><ref>{{cite journal | vauthors = Ewald CY, Landis JN, Porter Abate J, Murphy CT, Blackwell TK | title = Dauer-independent insulin/IGF-1-signalling implicates collagen remodelling in longevity | language = En | journal = Nature | volume = 519 | issue = 7541 | pages = 97–101 | date = March 2015 | pmid = 25517099 | pmc = 4352135 | doi = 10.1038/nature14021 | bibcode = 2015Natur.519...97E }}</ref> while glucose feeding promotes oxidative stress and reduces adult lifespan by a half.<ref name="ReferenceC"/> Similarly, induced degradation of an insulin/IGF-1 receptor late in life extended life expectancy of worms dramatically.<ref>{{Cite journal|last1=Venz|first1=Richard|last2=Pekec|first2=Tina|last3=Katic|first3=Iskra|last4=Ciosk|first4=Rafal|author5-link=Collin Y. Ewald|last5=Ewald|first5=Collin Yvès|date=2021-09-10|editor-last=Leiser|editor-first=Scott F|editor2-last=Kaeberlein|editor2-first=Matt|editor3-last=Alcedo|editor3-first=Joy|title=End-of-life targeted degradation of DAF-2 insulin/IGF-1 receptor promotes longevity free from growth-related pathologies|journal=eLife|volume=10|pages=e71335|doi=10.7554/eLife.71335|pmid=34505574|pmc=8492056|issn=2050-084X |doi-access=free }}</ref> 
Long-lived [[mutant]]s of ''C. elegans'' were demonstrated to be resistant to [[oxidative stress]] and [[ultraviolet|UV light]].<ref name="Hyun2008">{{Cite journal |doi=10.1093/nar/gkm1161 |pmc=2275101 |pmid=18203746|title=Longevity and resistance to stress correlate with DNA repair capacity in Caenorhabditis elegans |year=2008 |last1=Hyun |first1=Moonjung |last2=Lee |first2=Jihyun |last3=Lee |first3=Kyungjin |last4=May |first4=Alfred |last5=Bohr |first5=Vilhelm A. |last6=Ahn |first6=Byungchan |journal=Nucleic Acids Research |volume=36 |issue=4 |pages=1380–1389 }}</ref> These long-lived mutants had a higher [[DNA repair]] capability than wild-type ''C. elegans''.<ref name = Hyun2008/> Knockdown of the [[nucleotide excision repair]] gene Xpa-1 increased sensitivity to UV and reduced the [[longevity|life span]] of the long-lived mutants. These findings indicate that [[DNA damage theory of aging|DNA repair capability underlies longevity]].  Consistent with the idea that oxidative DNA damage causes aging, it was found that in ''C. elegans'', [[exosome (vesicle)|exosome]]-mediated delivery of [[superoxide dismutase]] (SOD) reduces the level of [[reactive oxygen species]] (ROS) and significantly extends lifespan, i.e. delays aging under normal, as well as hostile conditions.<ref>{{cite journal |vauthors=Shao X, Zhang M, Chen Y, Sun S, Yang S, Li Q |title=Exosome-mediated delivery of superoxide dismutase for anti-aging studies in Caenorhabditis elegans |journal=Int J Pharm |volume=641 |issue= |pages=123090 |date=June 2023 |pmid=37268030 |doi=10.1016/j.ijpharm.2023.123090 |url=}}</ref>

The capacity to repair DNA damage by the process of nucleotide excision repair declines with age.<ref>{{Cite journal |doi=10.1186/gb-2007-8-5-r70 |pmc=1929140 |pmid=17472752|title=Decline of nucleotide excision repair capacity in aging Caenorhabditis elegans |year=2007 |last1=Meyer |first1=Joel N. |last2=Boyd |first2=Windy A. |last3=Azzam |first3=Gregory A. |last4=Haugen |first4=Astrid C. |last5=Freedman |first5=Jonathan H. |last6=Van Houten |first6=Bennett |journal=Genome Biology |volume=8 |issue=5 |pages=R70 |doi-access=free }}</ref>

''C. elegans'' exposed to 5mM [[lithium chloride]] (LiCl) showed lengthened life spans.<ref>{{cite journal | vauthors = McColl G, Killilea DW, Hubbard AE, Vantipalli MC, Melov S, Lithgow GJ | title = Pharmacogenetic analysis of lithium-induced delayed aging in Caenorhabditis elegans | journal = The Journal of Biological Chemistry | volume = 283 | issue = 1 | pages = 350–7 | date = January 2008 | pmid = 17959600 | pmc = 2739662 | doi = 10.1074/jbc.M705028200 | doi-access = free }}</ref> When exposed to 10μM LiCl, reduced mortality was observed, but not with 1μM.<ref>{{cite journal | vauthors = Zarse K, Terao T, Tian J, Iwata N, Ishii N, Ristow M | title = Low-dose lithium uptake promotes longevity in humans and metazoans | journal = European Journal of Nutrition | volume = 50 | issue = 5 | pages = 387–9 | date = August 2011 | pmid = 21301855 | pmc = 3151375 | doi = 10.1007/s00394-011-0171-x }}</ref>

''C. elegans'' has been instrumental in the identification of the functions of genes implicated in [[Alzheimer's disease]], such as [[PSEN1|presenilin]].<ref>{{cite journal | vauthors = Ewald CY, Li C | title = Understanding the molecular basis of Alzheimer's disease using a Caenorhabditis elegans model system | journal = Brain Structure & Function | volume = 214 | issue = 2–3 | pages = 263–83 | date = March 2010 | pmid = 20012092 | pmc = 3902020 | doi = 10.1007/s00429-009-0235-3 }}</ref> Moreover, extensive research on ''C. elegans'' has identified [[RNA-binding protein]]s as essential factors during germline and early embryonic development.<ref>{{cite journal | vauthors = Hanazawa M, Yonetani M, Sugimoto A | title = PGL proteins self associate and bind RNPs to mediate germ granule assembly in C. elegans | journal = The Journal of Cell Biology | volume = 192 | issue = 6 | pages = 929–37 | date = March 2011 | pmid = 21402787 | pmc = 3063142 | doi = 10.1083/jcb.201010106 }}</ref>

[[Telomere]]s, the length of which have been shown to correlate with increased lifespan and delayed onset of [[senescence]] in a multitude of organisms, from ''C. elegans''<ref>{{Cite journal|last1=Coutts|first1=Fiona|last2=Palmos|first2=Alish B.|last3=Duarte|first3=Rodrigo R. R.|last4=de Jong|first4=Simone|last5=Lewis|first5=Cathryn M.|last6=Dima|first6=Danai|last7=Powell|first7=Timothy R.|date=March 2019|title=The polygenic nature of telomere length and the anti-ageing properties of lithium|journal=Neuropsychopharmacology|volume=44|issue=4|pages=757–765|doi=10.1038/s41386-018-0289-0|issn=1740-634X|pmc=6372618|pmid=30559463}}</ref><ref>{{Cite journal|last1=Raices|first1=Marcela|last2=Maruyama|first2=Hugo|last3=Dillin|first3=Andrew|last4=Karlseder|first4=Jan|date=September 2005|title=Uncoupling of longevity and telomere length in C. elegans|journal=PLOS Genetics|volume=1|issue=3|pages=e30|doi=10.1371/journal.pgen.0010030|issn=1553-7404|pmc=1200426|pmid=16151516 |doi-access=free }}</ref> to humans,<ref>{{Cite journal|last1=Lulkiewicz|first1=M.|last2=Bajsert|first2=J.|last3=Kopczynski|first3=P.|last4=Barczak|first4=W.|last5=Rubis|first5=B.|date=September 2020|title=Telomere length: how the length makes a difference|journal=Molecular Biology Reports|volume=47|issue=9|pages=7181–7188|doi=10.1007/s11033-020-05551-y|issn=1573-4978|pmc=7561533|pmid=32876842}}</ref> show an interesting behaviour in ''C. elegans.'' While ''C. elegans'' maintains its telomeres in a canonical way similar to other eukaryotes, in contrast ''[[Drosophila melanogaster]]'' is noteworthy in its use of [[retrotransposon]]s to maintain its telomeres,<ref>{{Cite journal|last1=Pardue|first1=Mary-Lou|last2=DeBaryshe|first2=P. G.|date=2011-12-20|title=Retrotransposons that maintain chromosome ends|journal=Proceedings of the National Academy of Sciences of the United States of America|volume=108|issue=51|pages=20317–20324|doi=10.1073/pnas.1100278108|issn=1091-6490|pmc=3251079|pmid=21821789|doi-access=free}}</ref> during [[Gene knockout|knock-out]] of the [[Telomerase reverse transcriptase|catalytic 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 canonical [[telomerase]] pathway.<ref>{{Cite journal|last1=Meier|first1=Bettina|last2=Clejan|first2=Iuval|last3=Liu|first3=Yan|last4=Lowden|first4=Mia|last5=Gartner|first5=Anton|last6=Hodgkin|first6=Jonathan|last7=Ahmed|first7=Shawn|date=February 2006|title=trt-1 is the Caenorhabditis elegans catalytic subunit of telomerase|journal=PLOS Genetics|volume=2|issue=2|pages=e18|doi=10.1371/journal.pgen.0020018|issn=1553-7404|pmc=1361356|pmid=16477310 |doi-access=free }}</ref> ALT is also observed in about 10-15% of all clinical cancers.<ref>{{Cite journal|last1=Cesare|first1=Anthony J.|last2=Reddel|first2=Roger R.|date=May 2010|title=Alternative lengthening of telomeres: models, mechanisms and implications|url=https://pubmed.ncbi.nlm.nih.gov/20351727|journal=Nature Reviews. Genetics|volume=11|issue=5|pages=319–330|doi=10.1038/nrg2763|issn=1471-0064|pmid=20351727|s2cid=19224032}}</ref> Thus ''C. elegans'' is a prime candidate for ALT research.<ref>{{Cite journal|last1=Ijomone|first1=Omamuyovwi M.|last2=Miah|first2=Mahfuzur R.|last3=Peres|first3=Tanara V.|last4=Nwoha|first4=Polycarp U.|last5=Aschner|first5=Michael|date=December 2016|title=Null allele mutants of trt-1, the catalytic subunit of telomerase in Caenorhabditis elegans, are less sensitive to Mn-induced toxicity and DAergic degeneration|url=https://pubmed.ncbi.nlm.nih.gov/27593554|journal=Neurotoxicology|volume=57|pages=54–60|doi=10.1016/j.neuro.2016.08.016|issn=1872-9711|pmid=27593554|bibcode=2016NeuTx..57...54I }}</ref><ref>{{Cite journal|last1=Shtessel|first1=Ludmila|last2=Lowden|first2=Mia Rochelle|last3=Cheng|first3=Chen|last4=Simon|first4=Matt|last5=Wang|first5=Kyle|last6=Ahmed|first6=Shawn|date=February 2013|title=Caenorhabditis elegans POT-1 and POT-2 repress telomere maintenance pathways|journal=G3: Genes, Genomes, Genetics|volume=3|issue=2|pages=305–313|doi=10.1534/g3.112.004440|issn=2160-1836|pmc=3564990|pmid=23390606}}</ref><ref>{{Cite journal|last1=Kwon|first1=Mi-Sun|last2=Min|first2=Jaewon|last3=Jeon|first3=Hee-Yeon|last4=Hwang|first4=Kwangwoo|last5=Kim|first5=Chuna|last6=Lee|first6=Junho|last7=Joung|first7=Je-Gun|last8=Park|first8=Woong-Yang|last9=Lee|first9=Hyunsook|date=October 2016|title=Paradoxical delay of senescence upon depletion of BRCA2 in telomerase-deficient worms|journal=FEBS Open Bio|volume=6|issue=10|pages=1016–1024|doi=10.1002/2211-5463.12109|issn=2211-5463|pmc=5055038|pmid=27761361}}</ref> Bayat et al. showed the paradoxical shortening of telomeres during ''[[Telomerase reverse transcriptase|trt-1]]'' [[over-expression]] which lead to near [[Sterility (physiology)|sterility]] while the worms even exhibited a slight increase in lifespan, despite shortened telomeres.<ref>{{Cite journal|last1=Bayat|first1=Melih|last2=Tanny|first2=Robyn E.|last3=Wang|first3=Ye|last4=Herden|first4=Carla|last5=Daniel|first5=Jens|last6=Andersen|first6=Erik C.|last7=Liebau|first7=Eva|last8=Waschk|first8=Daniel E. J.|date=2020-03-30|title=Effects of telomerase overexpression in the model organism Caenorhabditis elegans|url=https://pubmed.ncbi.nlm.nih.gov/31954861|journal=Gene|volume=732|pages=144367|doi=10.1016/j.gene.2020.144367|issn=1879-0038|pmid=31954861|s2cid=210829489}}</ref>

=== Sleep ===
''C. elegans'' is notable in [[non-human sleep|animal sleep]] studies as the most primitive organism to display sleep-like states. In ''C. elegans'', a [[fatigue (medical)|lethargus]] phase occurs shortly before each [[ecdysis|moult]].<ref>{{cite journal | vauthors = Iwanir S, Tramm N, Nagy S, Wright C, Ish D, Biron D | title = The microarchitecture of C. elegans behavior during lethargus: homeostatic bout dynamics, a typical body posture, and regulation by a central neuron | journal = Sleep | volume = 36 | issue = 3 | pages = 385–95 | date = March 2013 | pmid = 23449971 | pmc = 3571756 | doi = 10.5665/Sleep.2456 }}</ref> ''C. elegans'' has also been demonstrated to sleep after exposure to physical stress, including heat shock, UV radiation, and bacterial toxins.<ref>{{cite journal | vauthors = Hill AJ, Mansfield R, Lopez JM, Raizen DM, Van Buskirk C | title = Cellular stress induces a protective sleep-like state in C. elegans | journal = Current Biology | volume = 24 | issue = 20 | pages = 2399–405 | date = October 2014 | pmid = 25264259 | pmc = 4254280 | doi = 10.1016/j.cub.2014.08.040 | bibcode = 2014CBio...24.2399H }}</ref>

=== Sensory biology ===
While the worm has no eyes, it has been found to be sensitive to light due to a third type of light-sensitive animal [[photoreceptor protein]], [[LITE-1]], which is 10 to 100 times more efficient at absorbing light than the other two types of photopigments ([[opsins]] and [[cryptochromes]]) found in the animal kingdom.<ref>[https://www.livescience.com/56913-new-photoreceptor-found-in-worms.html Teensy, Eyeless Worms Have Completely New Light-Detecting Cells]</ref>

''C. elegans'' is remarkably adept at tolerating acceleration. It can withstand 400,000 [[g-force|g]]'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.<ref>Scientific American, August 2018, page 14</ref>

=== Drug library screening ===
Having a small size and short life cycle, C. elegans is one of the few organisms that can enable in vivo [[high throughput screening]] (HTS) platforms for the evaluation of chemical libraries of drugs and toxins in a multicellular organism.<ref>{{cite journal | title = In vivo quantitative high-throughput screening for drug discovery and comparative toxicology.|author1 = Dranchak, P.K.|author2 = Oliphant, E.|author3 = Queme, B. |author4 = Lamy, L. |author5 = Wang, Y.|author6 = Huang, R. |author7 = Xia, M. |author8 = Tao, D.|author9 = Inglese, J.| journal = Dis Model Mech|date = 2023 |volume = 16| issue=3 | pages=dmm049863 |doi = 10.1242/dmm.049863| pmid=36786055 |pmc = 10067442}}</ref> 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.<ref>{{cite journal | title = Caenorhabditis elegans for rare disease modeling and drug discovery: strategies and strengths. |author1 = Kropp, P.A. |author2 = Bauer, R.|author3 = Zafra, I. |author4 = Graham, C. |author5 = Golden, A.| journal = Dis Model Mech|date = 2021 |volume = 14|issue = 8 | pages = dmm049010|doi = 10.1242/dmm.049010|pmid = 34370008 |pmc = 8380043}}</ref>

=== Spaceflight research ===
''C. elegans'' made news when specimens were discovered to have survived the [[Space Shuttle Columbia disaster|Space Shuttle ''Columbia'' disaster]] in February 2003.<ref>
{{cite news
 |date=1 May 2003
 |title=Worms survived Columbia disaster
 |url=http://news.bbc.co.uk/1/hi/sci/tech/2992123.stm
 |work=BBC News
 |access-date=2008-07-11
}}</ref> Later, in January 2009, live samples of ''C. elegans'' from the [[University of Nottingham]] were announced to be spending two weeks on the [[International Space Station]] that October, in a [[space research]] project to explore the effects of [[zero gravity]] on muscle development and physiology. The research was primarily about genetic basis of [[muscle atrophy]], which relates to [[spaceflight]] or being bed-ridden, [[geriatric]], or [[diabetic]].<ref>
{{cite news
 |date=17 January 2009
 |title=University sends worms into space
 |url=http://news.bbc.co.uk/1/hi/england/nottinghamshire/7835020.stm
 |work=BBC News
 |access-date=2009-07-09
}}</ref> Descendants of the worms aboard Columbia in 2003 were launched into space on [[Space Shuttle Endeavour|''Endeavour'']] for the [[STS-134]] mission.<ref>{{cite news
 |last1=Klotz
 |first1=I
 |date=16 May 2011
 |title=Legacy Space Worms Flying on Shuttle
 |url=http://news.discovery.com/space/legacy-space-worms-flying-on-shuttle-110516.html
 |work=[[Discovery News]]
 |access-date=2011-05-17
 |archive-date=2012-06-16
 |archive-url=https://web.archive.org/web/20120616014937/http://news.discovery.com/space/legacy-space-worms-flying-on-shuttle-110516.html
 |url-status=dead
 }}</ref> Additional experiments on muscle dystrophy during spaceflight were carried on board the ISS starting in 2018.<ref>{{Cite journal |last1=Soni |first1=Purushottam |last2=Anupom |first2=Taslim |last3=Lesanpezeshki |first3=Leila |last4=Rahman |first4=Mizanur |last5=Hewitt |first5=Jennifer E. |last6=Vellone |first6=Matthew |last7=Stodieck |first7=Louis |last8=Blawzdziewicz |first8=Jerzy |last9=Szewczyk |first9=Nathaniel J. |last10=Vanapalli |first10=Siva A. |date=2022-11-07 |title=Microfluidics-integrated spaceflight hardware for measuring muscle strength of Caenorhabditis elegans on the International Space Station |journal=npj Microgravity |volume=8 |issue=1 |pages=50 |doi=10.1038/s41526-022-00241-4 |issn=2373-8065 |pmc=9640571 |pmid=36344513|bibcode=2022npjMG...8...50S }}</ref> 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.