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{{Short description|Condition in multi-cellular organisms}}
{{distinguish|Mosaic virus}}

[[File:Tulip with mosaicism.jpg|thumb|alt=Tulip flower with one side red and one side yellow.|Tulip flower showing mosaicism]]

'''Mosaicism''' or '''genetic mosaicism''' is a condition in which a [[multicellular organism]] possesses more than one [[lineage (genetic)|genetic line]] as the result of genetic [[mutation]].<ref name=":3">{{cite journal |last1=Campbell |first1=Ian M. |last2=Shaw |first2=Chad A. |last3=Stankiewicz |first3=Pawel |last4=Lupski |first4=James R. |title=Somatic mosaicism: implications for disease and transmission genetics |journal=Trends in Genetics |date=July 2015 |volume=31 |issue=7 |pages=382–392 |doi=10.1016/j.tig.2015.03.013 |pmc=4490042 |pmid=25910407 }}</ref><ref name=":4">{{cite journal |last1=Forsberg |first1=Lars A. |last2=Gisselsson |first2=David |last3=Dumanski |first3=Jan P. |title=Mosaicism in health and disease — clones picking up speed |journal=Nature Reviews Genetics |date=February 2017 |volume=18 |issue=2 |pages=128–142 |doi=10.1038/nrg.2016.145 |pmid=27941868 }}</ref> This means that various genetic lines resulted from a single [[fertilisation|fertilized]] [[egg cell|egg]]. Mosaicism is one of several possible causes of [[chimera (genetics)|chimerism]], wherein a single organism is composed of cells with more than one distinct [[genotype]].

Genetic mosaicism can result from many different mechanisms including chromosome [[nondisjunction]], [[anaphase lag]], and [[endoreplication]].<ref name="taylor2014">{{cite journal |last1=Taylor |first1=T. H. |last2=Gitlin |first2=S. A. |last3=Patrick |first3=J. L. |last4=Crain |first4=J. L. |last5=Wilson |first5=J. M. |last6=Griffin |first6=D. K. |year=2014 |title=The origin, mechanisms, incidence and clinical consequences of chromosomal mosaicism in humans |journal=Human Reproduction Update |volume=20 |issue=4 |pages=571–581 |doi=10.1093/humupd/dmu016 |pmid=24667481 |doi-access=free }}</ref> Anaphase lagging is the most common way by which mosaicism arises in the preimplantation embryo.<ref name=taylor2014/> Mosaicism can also result from a [[mutation]] in one cell during [[morphogenesis|development]], in which case the mutation will be passed on only to its daughter cells (and will be present only in certain adult cells).<ref name="Strachan 1999">{{cite book |last1=Strachan |first1=Tom |url=https://archive.org/details/humanmolecularge0002stra |title=Human Molecular Genetics |last2=Read |first2=Andrew P. |publisher=Wiley–Liss |year=1999 |isbn=978-1-85996-202-2 |edition=2nd |location=New York |chapter=Glossary |pmid=21089233 |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK7584/ |url-access=registration}}{{Page needed|date=January 2011}}</ref> Somatic mosaicism is not generally inheritable as it does not generally affect germ cells.<ref name=":4"/>

==History==
In 1929, [[Alfred Sturtevant]] studied mosaicism in ''[[Drosophila]]'', a genus of fruit fly.<ref name=":2">{{cite journal |last=Sturtevant |first=A. H. |date=1929 |title=The claret mutant type of Drosophila simulans: a study of chromosome elimination and cell-lineage |journal=Zeitschrift für Wissenschaftliche Zoologie |volume=135 |pages=323–356 |url={{GBurl|nKfPAAAAMAAJ|p=323}} }}</ref> H. J. Muller in 1930 demonstrated that mosaicism in ''Drosophila'' is always associated with [[chromosomal rearrangement]]s, and Schultz in 1936 showed that, in all cases studied, these rearrangements were associated with [[heterochromatic]] inert regions. Several hypotheses on the nature of such mosaicism were proposed. One hypothesis assumed that mosaicism appears as the result of a break and loss of chromosome segments. [[Curt Stern]] in 1935 assumed that the structural changes in the chromosomes took place as a result of ''somatic crossing'', as a result of which mutations or small chromosomal rearrangements in somatic cells. Thus the inert region causes an increase in mutation frequency or small chromosomal rearrangements in active segments adjacent to inert regions.<ref name="belgovskii44">{{cite journal |last1=Бельговский |first1=Марк Леонидович |title=К вопросу о механизме осуществления мозаичности, связанной с гетерохроматическими районами хромосом |language=ru |journal=Журнал общей биологии |volume=5 |issue=6 |date=1944 |pages=325–356 }} Translated as: {{cite book |last1=Belgovskii |first1=M. L. |date=1962 |title=The Causes of Mosaicism Associated With Heterochromatic Chromosome Regions |id=OTS 61-11476 |hdl=2027/mdp.39015086686659 |hdl-access=free }}</ref>

In the 1930s, Stern demonstrated that [[genetic recombination]], normal in [[meiosis]], can also take place in [[mitosis]].<ref name=stern31>{{cite journal |last1=Stern |first1=C |last2=Sekiguti |first2=K |date=1931 |title=Analyse eines Mosaikindividuums bei ''Drosophila melanogaster'' |trans-title=Analysis of a mosaic individual in ''Drosophila melanogaster'' |language=de |journal=Biologisches Zentralblatt |volume=51 |pages=194–199 }}</ref><ref name="stern36">{{cite journal |last1=Stern |first1=Curt |title=Somatic Crossing over and Segregation in Drosophila Melanogaster |journal=Genetics |date=November 1936 |volume=21 |issue=6 |pages=625–730 |doi=10.1093/genetics/21.6.625 |pmid=17246815 |pmc=1208727 }}</ref> When it does, it results in somatic (body) mosaics. These organisms contain two or more genetically distinct types of tissue.<ref name=Curt>{{cite book |last1=Stern |first1=Curt |chapter=Genetic mosaics in animals and man |pages=27–129 |title=Genetic Mosaics, and Other Essays |date=1968 |publisher=Harvard University Press |isbn=978-0-19-626451-6 }}</ref> The term ''somatic mosaicism'' was used by CW Cotterman in 1956 in his seminal paper on [[antigenic variation]].<ref name="De 2011 217–223">{{cite journal |last=De |first=S. |title=Somatic mosaicism in healthy human tissues |journal=Trends in Genetics |year=2011 |volume=27 |issue=6 |pages=217–223 |doi=10.1016/j.tig.2011.03.002 |pmid=21496937}}</ref>

In 1944, [[:ru:Бельговский, Марк Леонидович|M. L. Belgovskii]] proposed that mosaicism could not account for certain mosaic expressions caused by chromosomal rearrangements involving heterochromatic inert regions. The associated weakening of biochemical activity led to what he called a ''[[chimera (genetics)|genetic chimera]]''.{{psc|date=July 2025}}<ref name=belgovskii44/>

==Types==

===Germline mosaicism===
{{Main|Germline mosaicism}}
Germline or gonadal mosaicism is a particular form of mosaicism wherein some [[gamete]]s—i.e., [[sperm]] or [[oocyte]]s—carry a mutation, but the rest are normal.<ref>{{cite web |title=Google Health – Google |url=https://health.google.com/health/ref/Mosaicism |website=health.google.com}}</ref><ref>{{cite journal |last1=Schwab |first1=Angela L. |display-authors=etal |year=2007 |title=Gonadal mosaicism and familial adenomatous polyposis |journal=Familial Cancer |volume=7 |issue=2 |pages=173–7 |doi=10.1007/s10689-007-9169-1 |pmid=18026870 }}</ref> The cause is usually a mutation that occurred in an early stem cell that gave rise to all or part of the gametes.

===Somatic mosaicism===
Somatic mosaicism (also known as clonal mosaicism) occurs when the [[somatic cell]]s of the body are of more than one genotype. In the more common mosaics, different genotypes arise from a single fertilized egg cell, due to [[mitotic]] errors at first or later cleavages.

Somatic mutation leading to mosaicism is prevalent in the beginning and end stages of human life.<ref name="De 2011 217–223"/> Somatic mosaics are common in [[embryogenesis]] due to [[retrotransposition]] of [[LINE1|long interspersed nuclear element-1]] (LINE-1 or L1) and [[Alu element|Alu]] [[transposable element]]s.<ref name="De 2011 217–223"/> In early development, DNA from undifferentiated cell types may be more susceptible to mobile element invasion due to long, [[DNA methylation|unmethylated]] regions in the genome.<ref name="De 2011 217–223"/> Further, the accumulation of DNA copy errors and damage over a lifetime lead to greater occurrences of mosaic tissues in aging humans. As longevity has increased dramatically over the last century, human genome may not have had time to adapt to cumulative effects of [[mutagenesis]].<ref name="De 2011 217–223"/> Thus, [[cancer research]] has shown that somatic mutations are increasingly present throughout a lifetime and are responsible for most [[leukemia]], [[lymphoma]]s, and solid tumors.<ref>{{cite journal |last=Jacobs |first=K. B. |display-authors=etal |year=2012 |title=Detectable Clonal Mosaicism and Its Relationship to Aging and Cancer |journal=Nature Genetics |volume=44 |issue=6 |pages=651–U668 |doi=10.1038/ng.2270 |pmc=3372921 |pmid=22561519}}</ref>

====Trisomies, monosomies, and related conditions====
The most common form of mosaicism found through prenatal diagnosis involves [[trisomy|trisomies]]. Although most forms of trisomy are due to problems in [[meiosis]] and affect all cells of the organism, some cases occur where the trisomy occurs in only a selection of the cells. This may be caused by a nondisjunction event in an early mitosis, resulting in a loss of a chromosome from some trisomic cells.<ref>{{cite book |first1=Tom |last1=Strachan |first2=Andrew P. |last2=Read |year=1999 |chapter=Chromosome abnormalities |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK7572/#A196 |title=Human Molecular Genetics |edition=2nd |location=New York |publisher=Wiley–Liss |isbn=978-1-85996-202-2 |pmid=21089233 |url-access=registration |url=https://archive.org/details/humanmolecularge0002stra}}{{Page needed|date=January 2011}}</ref> Generally, this leads to a milder [[phenotype]] than in nonmosaic patients with the same disorder.

In rare cases, [[intersex]] conditions can be caused by mosaicism where some cells in the body have [[sex-determination system|XX]] and others XY chromosomes ([[46, XX/XY]]).<ref>{{cite journal |last1=Marchi |first1=M. De |display-authors=etal |year=2008 |title=True hermaphroditism with XX/XY sex chromosome mosaicism: Report of a case |journal=Clinical Genetics |volume=10 |issue=5 |pages=265–72 |doi=10.1111/j.1399-0004.1976.tb00047.x |pmid=991437 }}</ref><ref>{{cite journal |last1=Fitzgerald |first1=P. H. |last2=Donald |first2=R. A. |last3=Kirk |first3=R. L. |year=1979 |title=A true hermaphrodite dispermic chimera with 46,XX and 46,XY karyotypes |journal=Clinical Genetics |volume=15 |issue=1 |pages=89–96 |doi=10.1111/j.1399-0004.1979.tb02032.x |pmid=759058 }}</ref> In the fruit fly ''[[Drosophila melanogaster]]'', where a fly possessing two X chromosomes is a female and a fly possessing a single X chromosome is a sterile male, a loss of an X chromosome early in embryonic development can result in sexual mosaics, or [[gynandromorphism|gynandromorphs]].<ref name=":2"/><ref name=":0"/> Likewise, a loss of the [[Y chromosome]] can result in XY/X mosaic males.<ref name=":1"/>

An example of this is one of the milder forms of [[Klinefelter syndrome]], called 46,XY/47,XXY mosaic wherein some of the patient's cells contain XY chromosomes, and some contain XXY chromosomes. The 46/47 annotation indicates that the XY cells have the normal number of 46 total chromosomes, and the XXY cells have a total of 47 chromosomes.

Also [[monosomy|monosomies]] can present with some form of mosaicism. The only non-lethal full monosomy occurring in humans is the one causing [[Turner's syndrome]]. Around 30% of Turner's syndrome cases demonstrate mosaicism, while complete monosomy (45, X) occurs in about 50–60% of cases.

Mosaicism isn't necessarily deleterious, though. Revertant somatic mosaicism is a rare recombination event with a spontaneous correction of a mutant, [[pathogenic allele]].<ref name="Jongmans 2012 426–433">{{cite journal |last=Jongmans |first=M. C. J. |title=Revertant somatic mosaicism by mitotic recombination in Dyskeratosis Congenita |journal=American Journal of Human Genetics |year=2012 |volume=90 |issue=3 |pages=426–433 |doi=10.1016/j.ajhg.2012.01.004 |display-authors=etal |pmid=22341970 |pmc=3309184}}</ref> In revertant mosaicism, the healthy tissue formed by mitotic recombination can outcompete the original, surrounding mutant cells in tissues such as [[blood]] and [[epithelium|epithelia]] that regenerate often.<ref name="Jongmans 2012 426–433"/> In the skin disorder [[ichthyosis with confetti]], normal skin spots appear early in life and increase in number and size over time.<ref name="Jongmans 2012 426–433"/>

Other endogenous factors can also lead to mosaicism, including [[mobile genetic elements|mobile elements]], [[DNA polymerase]] slippage, and unbalanced [[chromosome segregation]].<ref name="De 2011 217–223"/> Exogenous factors include [[nicotine]] and [[ultraviolet|UV radiation]].<ref name="De 2011 217–223"/> Somatic mosaics have been created in ''Drosophila'' using X‑ray treatment and the use of [[irradiation]] to induce somatic mutation has been a useful technique in the study of genetics.<ref>{{cite journal |last=Blair |first=S. S. |title=Genetic mosaic techniques for studying Drosophila development |journal=Development |volume=130 |issue=21 |pages=5065–5072 |doi=10.1242/dev.00774 |pmid=12975340 |year=2003 |doi-access=free}}</ref>

True mosaicism should not be mistaken for the phenomenon of [[X-inactivation]], where all cells in an organism have the same genotype, but a different copy of the X chromosome is expressed in different cells. The latter is the case in normal (XX) female mammals, although it is not always visible from the phenotype (as it is in [[calico cat]]s). However, all [[multicellular organism]]s are likely to be somatic mosaics to some extent.<ref name="Hall 1988 355–363">{{cite journal |last=Hall |first=J. G. |title=Review and hypotheses: Somatic mosaicism, observations related to clinical genetics |journal=American Journal of Human Genetics |year=1988 |volume=43 |issue=4 |pages=355–363 |pmid=3052049 |pmc=1715487}}</ref>

====Gonosomal mosaicism====
Gonosomal mosaicism is a type of somatic mosaicism that occurs very early in the organisms development and thus is present within both germline and somatic cells.<ref name=":3"/><ref name=":5">{{cite journal |display-authors=3 |last1=Mensa-Vilaró |first1=Anna |last2=Bravo García-Morato |first2=María |last3=de la Calle-Martin |first3=Oscar |last4=Franco-Jarava |first4=Clara |last5=Martínez-Saavedra |first5=María Teresa |last6=González-Granado |first6=Luis I. |last7=González-Roca |first7=Eva |last8=Fuster |first8=Jose Luis |last9=Alsina |first9=Laia |last10=Mutchinick |first10=Osvaldo M. |last11=Balderrama-Rodríguez |first11=Angélica |last12=Ramos |first12=Eduardo |last13=Modesto |first13=Consuelo |last14=Mesa-del-Castillo |first14=Pablo |last15=Ortego-Centeno |first15=Norberto |last16=Clemente |first16=Daniel |last17=Souto |first17=Alejandro |last18=Palmou |first18=Natalia |last19=Remesal |first19=Agustín |last20=Leslie |first20=Kieron S. |last21=Gómez de la Fuente |first21=Enrique |last22=Yadira Bravo Gallego |first22=Luz |last23=Campistol |first23=Josep María |last24=Dhouib |first24=Naouel Guirat |last25=Bejaoui |first25=Mohamed |last26=Dutra |first26=Lívia Almeida |last27=Terreri |first27=Maria Teresa |last28=Mosquera |first28=Catalina |last29=González |first29=Tatiana |last30=Cañellas |first30=Jerónima |last31=García-Ruiz de Morales |first31=José María |last32=Wouters |first32=Carine H. |last33=Bosque |first33=María Teresa |last34=Cham |first34=Weng Tarng |last35=Jiménez-Treviño |first35=Santiago |last36=de Inocencio |first36=Jaime |last37=Bloomfield |first37=Markéta |last38=Pérez de Diego |first38=Rebeca |last39=Martínez-Pomar |first39=Natalia |last40=Rodríguez-Pena |first40=Rebeca |last41=González-Santesteban |first41=Cecilia |last42=Soler-Palacín |first42=Pere |last43=Casals |first43=Ferran |last44=Yagüe |first44=Jordi |last45=Allende |first45=Luis M. |last46=Rodríguez-Gallego |first46=José Carlos |last47=Colobran |first47=Roger |last48=Martínez-Martínez |first48=Laura |last49=López-Granados |first49=Eduardo |last50=Aróstegui |first50=Juan I. |title=Unexpected relevant role of gene mosaicism in patients with primary immunodeficiency diseases |journal=Journal of Allergy and Clinical Immunology |date=January 2019 |volume=143 |issue=1 |pages=359–368 |doi=10.1016/j.jaci.2018.09.009 |pmid=30273710 |hdl=10668/13014 |hdl-access=free }}</ref> Somatic mosaicism is not generally inheritable as it does not usually affect germ cells. In the instance of gonosomal mosaicism, organisms have the potential to pass the genetic alteration, including to potential offspring because the altered allele is present in both somatic and germline cells.<ref name=":5"/>

====Brain cell mosaicism====
{{See also|Human somatic variation#Human somatic variations in brain}}
A frequent type of neuronal genomic mosaicism is [[copy number variation]]. Possible sources of such variation were suggested to be incorrect [[DNA repair|repairs of DNA damage]] and [[somatic recombination]].<ref name="pmid30464338">{{cite journal |vauthors=Lee MH, Siddoway B, Kaeser GE, Segota I, Rivera R, Romanow WJ, Liu CS, Park C, Kennedy G, Long T, Chun J |title=Somatic APP gene recombination in Alzheimer's disease and normal neurons |journal=Nature |volume=563 |issue=7733 |pages=639–645 |date=November 2018 |pmid=30464338 |doi=10.1038/s41586-018-0718-6 |bibcode=2018Natur.563..639L |pmc=6391999}}</ref>

====Mitotic recombination====
One basic mechanism that can produce mosaic tissue is [[mitotic recombination]] or [[mitotic crossover|somatic crossover]]. It was first discovered by [[Curt Stern]] in ''[[Drosophila]]'' in 1936. The amount of tissue that is mosaic depends on where in the tree of cell division the exchange takes place. A phenotypic character called "twin spot" seen in ''Drosophila'' is a result of mitotic recombination. However, it also depends on the allelic status of the genes undergoing recombination. Twin spot occurs only if the heterozygous genes are linked in repulsion, i.e. the trans phase. The recombination needs to occur between the centromeres of the adjacent gene. This gives an appearance of yellow patches on the wild-type background in ''Drosophila''. another example of mitotic recombination is the Bloom's syndrome, which happens due to the mutation in the ''blm'' gene. The resulting BLM protein is defective. The defect in [[RecQ helicase|RecQ]], a [[helicase]], facilitates the defective unwinding of DNA during replication, thus is associated with the occurrence of this disease.<ref>{{cite book |last1=King |first1=Robert C. |last2=Mulligan |first2=Pamela K. |last3=Stansfield |first3=William D. |title=A Dictionary of Genetics |date=2013 |doi=10.1093/acref/9780199766444.001.0001 |isbn=978-0-19-976644-4 |chapter=helicase |chapter-url={{GBurl|5jhH0HTjEdkC|p=209}} |page=209 }}</ref><ref>{{cite book |last1=Langer |first1=Katherine |last2=Cunniff |first2=Christopher M. |last3=Kucine |first3=Nicole |title=GeneReviews® |date=1993 |publisher=University of Washington, Seattle |chapter-url=https://www.ncbi.nlm.nih.gov/books/NBK1398/ |chapter=Bloom Syndrome |pmid=20301572 }}</ref>

==Use in experimental biology==
Genetic mosaics are a particularly powerful tool when used in the commonly studied [[Drosophila melanogaster|fruit fly]], where specially selected strains frequently lose an X<ref name=":0">{{cite journal |date=1972 |title=Mapping of Behaviour in Drosophila mosaics |journal=Nature |volume=240 |issue=5383 |pages=527–535 |doi=10.1038/240527a0 |last1=Hotta |first1=Yoshiki |last2=Benzer |first2=Seymour |bibcode=1972Natur.240..527H |pmid=4568399 }}</ref> or a Y<ref name=":1">{{cite journal |last=Nissani |first=Moti |date=1978 |title=The site of function of the Y chromosome in Drosophila melanogaster males |journal=Molecular and General Genetics |volume=165 |issue=2 |pages=221–224 |doi=10.1007/BF00269910 }}</ref> chromosome in one of the first embryonic cell divisions. These mosaics can then be used to analyze such things as courtship behavior,<ref name=":0"/> and female sexual attraction.<ref>{{cite journal |title=A new behavioral bioassay for an analysis of sexual attraction and pheromones in insects |journal=Journal of Experimental Zoology |volume=192 |issue=2 |pages=271–5 |doi=10.1002/jez.1401920217 |pmid=805823 |year=1975 |last1=Nissani |first1=M|bibcode=1975JEZ...192..271N }}</ref>

More recently, the use of a [[transgene]] incorporated into the ''Drosophila'' genome has made the system far more flexible. The [[FLP-FRT recombination|flip recombinase (or ''FLP'')]] is a gene from the commonly studied yeast ''[[Saccharomyces cerevisiae]]'' that recognizes "flip recombinase target" (FRT) sites, which are short sequences of DNA, and induces [[genetic recombination|recombination]] between them. FRT sites have been inserted transgenically near the [[centromere]] of each chromosome arm of ''D. melanogaster''. The ''FLP'' gene can then be induced selectively, commonly using either the heat shock promoter or the [[GAL4/UAS system]]. The resulting clones can be identified either negatively or positively.

In negatively marked clones, the fly is [[transheterozygote|transheterozygous]] for a gene encoding a visible marker (commonly the [[green fluorescent protein]]) and an allele of a gene to be studied (both on chromosomes bearing FRT sites). After induction of ''FLP'' expression, cells that undergo recombination will have progeny homozygous for either the marker or the allele being studied. Therefore, the cells that do not carry the marker (which are dark) can be identified as carrying a mutation.

Using negatively marked clones is sometimes inconvenient, especially when generating very small patches of cells, where seeing a dark spot on a bright background is more difficult than a bright spot on a dark background. Creating positively marked clones is possible using the so-called [[MARCM]] ("mosaic analysis with a repressible cell marker" system, developed by [[Liqun Luo]], a professor at [[Stanford University]], and his postdoctoral student Tzumin Lee, who now leads a group at [[Janelia Farm Research Campus]]. This system builds on the GAL4/UAS system, which is used to express GFP in specific cells. However, a globally expressed ''[[GAL80]]'' gene is used to repress the action of GAL4, preventing the expression of GFP. Instead of using GFP to mark the wild-type chromosome as above, GAL80 serves this purpose, so that when it is removed by [[mitotic recombination]], GAL4 is allowed to function, and GFP turns on. This results in the cells of interest being marked brightly in a dark background.<ref>{{cite journal |last1=Lee |first1=Tzumin |last2=Luo |first2=Liqun |title=Mosaic analysis with a repressible cell marker for studies of gene function in neuronal morphogenesis |journal=Neuron |volume=22 |issue=3 |pages=451–61 |year=1999 |pmid=10197526 |doi=10.1016/S0896-6273(00)80701-1 |doi-access=free}}</ref>

==See also==
* [[45,X/46,XY mosaicism]] (X0/XY mosaicism)

==References==
{{Reflist}}

==Further reading==
*{{cite news |title=Every Cell in Your Body Has the Same DNA. Except It Doesn't |last1=Zimmer |first1=Carl |newspaper=The New York Times |date=21 May 2018 |url=https://www.nytimes.com/2018/05/21/science/mosaicism-dna-genome-cancer.html |access-date=23 May 2018 |url-status=live |archive-url=https://web.archive.org/web/20180523011645/https://www.nytimes.com/2018/05/21/science/mosaicism-dna-genome-cancer.html |archive-date=23 May 2018}}
*{{cite web |title=From Many, One -- Diverse mammals, including humans, have been found to carry distinct genomes in their cells. What does such genetic chimerism mean for health and disease? |url=https://www.the-scientist.com/features/from-many-one-35710 |website=The Scientist |access-date=23 May 2018 |url-status=live |archive-url=https://web.archive.org/web/20170425031440/https://www.the-scientist.com/?articles.view%2FarticleNo%2F42476%2Ftitle%2FFrom-Many--One%2F |archive-date=25 April 2017}}

{{Chromosomal abnormalities}}

[[Category:Genetics]]
[[Category:Cell biology]]

Mosaic (genetics) - История изменений

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