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{{Short description| | {{Short description|Variant of DNA sequence at a locus}} | ||
{{Use dmy dates|date=July 2020}} | {{Use dmy dates|date=July 2020}} | ||
An '''allele'''{{refn|{{IPAc-en|UK|ˈ|æ|l|iː|l|,_|ə|ˈ|l|iː|l}}; modern formation from Greek ἄλλος ''állos'', "other"}} is a variant of the sequence of | An '''allele'''{{refn|{{IPAc-en|UK|ˈ|æ|l|iː|l|,_|ə|ˈ|l|iː|l}}; modern formation from Greek ἄλλος ''állos'', "other"}} is a variant of the sequence of nucleotides at a particular location, or locus, on a DNA molecule.<ref>{{ cite book | last = Graur | first = D | title = Molecular and Genome Evolution | publisher = Sinauer Associates, Inc. | place = Sunderland MA (USA) | date = 2016 }}</ref> | ||
Alleles can differ at a single position through [[ | Alleles can differ at a single position through [[single-nucleotide polymorphism]]s,<ref>{{Cite journal|last1=Smigielski|first1=Elizabeth M.|last2=Sirotkin|first2=Karl|last3=Ward|first3=Minghong|last4=Sherry|first4=Stephen T.|date=2000-01-01|title=dbSNP: a database of single nucleotide polymorphisms|journal=Nucleic Acids Research|volume=28|issue=1|pages=352–355|issn=0305-1048|pmid=10592272|pmc=102496|doi=10.1093/nar/28.1.352}}</ref> but they can also have insertions and deletions of up to several thousand base pairs.<ref>{{Cite book|last1=Elston|first1=Robert|last2=Satagopan|first2=Jaya|last3=Sun|first3=Shuying|date=2012|chapter=Genetic Terminology|series=Methods in Molecular Biology|volume=850|pages=1–9|doi=10.1007/978-1-61779-555-8_1|issn=1064-3745|pmc=4450815|pmid=22307690|title=Statistical Human Genetics|isbn=978-1-61779-554-1}}</ref> Most alleles result in little or no change in the characteristics of an individual organism but sometimes different alleles can result in different observable phenotypic traits such as antibiotic resistance in bacteria, developmental mutations in fruit flies, and genetic diseases in humans. | ||
Nearly all multicellular organisms have two sets of chromosomes at some point in their biological life cycle; that is, they are [[diploid]]. For a given locus, if the two chromosomes contain the same allele, they, and the organism, are homozygous with respect to that allele. If the alleles are different, they, and the organism, are heterozygous with respect to those alleles. A notable example of this is [[Gregor Mendel]]'s discovery that the white and purple flower colors in [[pea]] plants were the result of a single [[gene]] with two alleles. Mendel's discovery of what are now known as alleles resulted in three laws that help understand how alleles are passed on to progeny.<ref>{{Cite journal|title=Gregor Johann Mendel and the development of modern evolutionary biology|journal=Proceedings of the National Academy of Sciences of the United States of America|date=2022-07-26|issn=1091-6490|pmc=9335310|pmid=35858454|article-number=e2201327119|volume=119|issue=30|doi=10.1073/pnas.2201327119|first1=Nils Chr|last1=Stenseth|first2=Leif|last2=Andersson|first3=Hopi E.|last3=Hoekstra |bibcode=2022PNAS..11901327S |doi-access=free }}</ref> | |||
Popular definitions of 'allele' typically refer only to different alleles within genes. For example, the [[ABO blood group system|ABO blood grouping]] is controlled by the [[ABO (gene)|ABO gene]], which has six common alleles (variants). In [[population genetics]], nearly every living human's phenotype for the ABO gene is some combination of just these six alleles.<ref>{{cite journal | vauthors = Seltsam A, Hallensleben M, Kollmann A, Blasczyk R | title = The nature of diversity and diversification at the ABO locus | journal = Blood | volume = 102 | issue = 8 | pages = 3035–42 | date = October 2003 | pmid = 12829588 | doi = 10.1182/blood-2003-03-0955 | doi-access = free }}</ref><ref>{{cite journal | vauthors = Ogasawara K, Bannai M, Saitou N, Yabe R, Nakata K, Takenaka M, Fujisawa K, Uchikawa M, Ishikawa Y, Juji T, Tokunaga K | title = Extensive polymorphism of ABO blood group gene: three major lineages of the alleles for the common ABO phenotypes | journal = Human Genetics | volume = 97 | issue = 6 | pages = 777–83 | date = June 1996 | pmid = 8641696 | doi = 10.1007/BF02346189 | s2cid = 12076999 }}</ref> | |||
Popular definitions of 'allele' typically refer only to different alleles within genes. For example, the [[ABO blood group system|ABO blood grouping]] is controlled by the [[ABO (gene)|ABO gene]], which has six common alleles (variants). In [[population genetics]], nearly every living human's | |||
==Etymology== | ==Etymology== | ||
The word "allele" is a short form of "allelomorph" ("other form", a word coined by British geneticists [[William Bateson]] and [[Edith Rebecca Saunders]] | The word "allele" is a short form of "allelomorph" ("other form", a word coined by British geneticists [[William Bateson]] and [[Edith Rebecca Saunders]] in the early 1900s),<ref>{{cite web | last = Craft | first = Jude | title = Genes and genetics: the language of scientific discovery | work = Genes and genetics | publisher = [[Oxford English Dictionary]] | date = 2013 | url = http://public.oed.com/aspects-of-english/shapers-of-english/genes-and-genetics-the-language-of-scientific-discovery/ | access-date = 2016-01-14 | archive-date = 29 January 2018 | archive-url = https://web.archive.org/web/20180129140501/http://public.oed.com/aspects-of-english/shapers-of-english/genes-and-genetics-the-language-of-scientific-discovery/ | url-status = live }}</ref><ref>Bateson, W. and Saunders, E. R. (1902) "The facts of heredity in the light of Mendel's discovery." Reports to the Evolution Committee of the Royal Society, '''I.''' pp. 125–160</ref> which was used in the early days of [[genetics]] to describe variant forms of a [[gene]] detected in different [[phenotypes]] and identified to cause the differences between them. It derives from the [[Greek language|Greek]] prefix ἀλληλο-, ''allelo-'', meaning "mutual", "reciprocal", or "each other", which itself is related to the Greek adjective ἄλλος, ''allos'' (cognate with [[Latin]] ''alius''), meaning "other". | ||
==Alleles that lead to dominant or recessive phenotypes== | ==Alleles that lead to dominant or recessive phenotypes== | ||
{{main|Dominance (genetics)}} | {{main|Dominance (genetics)}} | ||
In many cases, genotypic interactions between the two alleles at a locus can be described as [[Dominance (genetics)|dominant]] or [[recessive]], according to which of the two homozygous phenotypes the [[heterozygote]] most resembles. Where the heterozygote is indistinguishable from one of the homozygotes, the allele expressed is the one that leads to the "dominant" phenotype,<ref name="Essential genetics: A genomics perspective"/><ref name="pmid 28696921">{{cite journal|date=September 2017|title=ASPsiRNA: A Resource of ASP-siRNAs Having Therapeutic Potential for Human Genetic Disorders and Algorithm for Prediction of Their Inhibitory Efficacy|journal=G3|volume=7|issue=9|pages=2931–2943|doi=10.1534/g3.117.044024|pmid=28696921|doi-access=free |last1=Monga |first1=Isha |last2=Qureshi |first2=Abid |last3=Thakur |first3=Nishant |last4=Gupta |first4=Amit Kumar |last5=Kumar |first5=Manoj |pmc=5592921 }}</ref> and the other allele is said to be "recessive". The degree and pattern of dominance varies among loci. This type of interaction was first formally-described by [[Gregor Mendel]]. However, many traits defy this simple categorization and the phenotypes are modelled by [[co-dominance]] and [[Quantitative trait locus|polygenic inheritance]].<ref>{{Cite web|url=https://www.genome.gov/genetics-glossary/Allele|title=Allele|website=Genome.gov|access-date=3 July 2021|archive-date=28 June 2021|archive-url=https://web.archive.org/web/20210628215931/https://www.genome.gov/genetics-glossary/Allele|url-status=live}}</ref> | In many cases, genotypic interactions between the two alleles at a locus can be described as [[Dominance (genetics)|dominant]] or [[recessive]], according to which of the two homozygous phenotypes the [[heterozygote]] most resembles. Where the heterozygote is indistinguishable from one of the homozygotes, the allele expressed is the one that leads to the "dominant" phenotype,<ref name="Essential genetics: A genomics perspective"/><ref name="pmid 28696921">{{cite journal|date=September 2017|title=ASPsiRNA: A Resource of ASP-siRNAs Having Therapeutic Potential for Human Genetic Disorders and Algorithm for Prediction of Their Inhibitory Efficacy|journal=G3|volume=7|issue=9|pages=2931–2943|doi=10.1534/g3.117.044024|pmid=28696921|doi-access=free |last1=Monga |first1=Isha |last2=Qureshi |first2=Abid |last3=Thakur |first3=Nishant |last4=Gupta |first4=Amit Kumar |last5=Kumar |first5=Manoj |pmc=5592921 }}</ref> and the other allele is said to be "recessive". In the case of a heterozygote, the dominant allele will mask the effect of the recessive allele, giving a dominant phenotype.<ref>{{Cite web|title=Dominant Traits and Alleles|url=https://www.genome.gov/genetics-glossary/Dominant-Traits-and-Alleles|website=www.genome.gov|access-date=2025-12-01|language=en}}</ref> The phenotype of recessive alleles are observable when an organism is homozygous recessive for a gene.<ref>{{Cite web|title=Recessive Traits and Alleles|url=https://www.genome.gov/genetics-glossary/Recessive-Traits-Alleles|website=www.genome.gov|access-date=2025-12-01|language=en}}</ref> The degree and pattern of dominance varies among loci. This type of interaction was first formally-described by [[Gregor Mendel]]. However, many traits defy this simple categorization and the phenotypes are modelled by [[co-dominance]] and [[Quantitative trait locus|polygenic inheritance]].<ref>{{Cite web|url=https://www.genome.gov/genetics-glossary/Allele|title=Allele|website=Genome.gov|access-date=3 July 2021|archive-date=28 June 2021|archive-url=https://web.archive.org/web/20210628215931/https://www.genome.gov/genetics-glossary/Allele|url-status=live}}</ref> | ||
The term "[[wild type]]" allele is sometimes used to describe an allele that is thought to contribute to the typical phenotypic character as seen in "wild" populations of organisms, such as fruit flies (''[[Drosophila melanogaster]]''). Such a "wild type" allele was historically regarded as leading to a dominant (overpowering – always expressed), common, and normal phenotype, in contrast to "[[mutant]]" alleles that lead to recessive, rare, and frequently deleterious phenotypes. It was formerly thought that most individuals were homozygous for the "wild type" allele at most gene loci, and that any alternative "mutant" allele was found in homozygous form in a small minority of "affected" individuals, often as [[genetic diseases]], and more frequently in heterozygous form in "[[Genetic carrier|carriers]]" for the mutant allele. It is now appreciated that most or all gene loci are highly polymorphic, with multiple alleles, whose frequencies vary from population to population, and that a great deal of genetic variation is hidden in the form of alleles that do not produce obvious phenotypic differences. Wild type alleles are often denoted by a superscript plus sign (''i.e.'', ''p{{sup|+}}'' for an allele ''p'').<ref>{{cite book|title = Genetics A Conceptual Approach|edition = 7|author = B. A. Pierce|publisher = Macmillan|date = 2020|isbn = 978-1-319-21680-1|page = 60}}</ref> | The term "[[wild type]]" allele is sometimes used to describe an allele that is thought to contribute to the typical phenotypic character as seen in "wild" populations of organisms, such as fruit flies (''[[Drosophila melanogaster]]''). Such a "wild type" allele was historically regarded as leading to a dominant (overpowering – always expressed), common, and normal phenotype, in contrast to "[[mutant]]" alleles that lead to recessive, rare, and frequently deleterious phenotypes. It was formerly thought that most individuals were homozygous for the "wild type" allele at most gene loci, and that any alternative "mutant" allele was found in homozygous form in a small minority of "affected" individuals, often as [[genetic diseases]], and more frequently in heterozygous form in "[[Genetic carrier|carriers]]" for the mutant allele. It is now appreciated that most or all gene loci are highly polymorphic, with multiple alleles, whose frequencies vary from population to population, and that a great deal of genetic variation is hidden in the form of alleles that do not produce obvious phenotypic differences. Wild type alleles are often denoted by a superscript plus sign (''i.e.'', ''p{{sup|+}}'' for an allele ''p'').<ref>{{cite book|title = Genetics A Conceptual Approach|edition = 7|author = B. A. Pierce|publisher = Macmillan|date = 2020|isbn = 978-1-319-21680-1|page = 60}}</ref> | ||
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==Genotype frequencies== | ==Genotype frequencies== | ||
{{main|Allele frequency}} | {{main|Allele frequency}} | ||
The frequency of alleles in a diploid population can be used to predict the frequencies of the corresponding genotypes (see [[Hardy–Weinberg principle]]). For a simple model, with two alleles; | The frequency of alleles in a diploid population can be used to predict the frequencies of the corresponding genotypes (see [[Hardy–Weinberg principle]]). For a simple model, with two alleles; | ||
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: <math>p^2 + 2pq + q^2=1 \,</math> | : <math>p^2 + 2pq + q^2=1 \,</math> | ||
where ''p'' is the frequency of one allele and ''q'' is the frequency of the alternative allele, which necessarily sum to unity. Then, ''p''<sup>2</sup> is the fraction of the population homozygous for the first allele, 2''pq'' is the fraction of heterozygotes, and ''q''<sup>2</sup> is the fraction homozygous for the alternative allele. If the first allele is dominant to the second then the fraction of the population that will show the dominant phenotype is ''p''<sup>2</sup> + 2''pq'', and the fraction with the recessive phenotype is ''q''<sup>2</sup>. | where ''p'' is the frequency of one allele and ''q'' is the frequency of the alternative allele, which necessarily sum to unity. Then, ''p''<sup>2</sup> is the fraction of the population homozygous for the first allele, 2''pq'' is the fraction of heterozygotes, and ''q''<sup>2</sup> is the fraction homozygous for the alternative allele. If the first allele is dominant to the second then the fraction of the population that will show the dominant phenotype is ''p''<sup>2</sup> + 2''pq'', and the fraction with the recessive phenotype is ''q''<sup>2</sup>.<ref>{{Cite web|title=Archived {{!}} Population Genetics and Statistics for Forensic Analysts {{!}} Hardy-Weinberg Principle {{!}} National Institute of Justice|url=https://nij.ojp.gov/nij-hosted-online-training-courses/population-genetics-and-statistics-forensic-analysts/population-theory/hardy-weinberg-principle|website=nij.ojp.gov|access-date=2025-12-01|language=en}}</ref> | ||
With three alleles: | With three alleles: | ||
| Line 59: | Line 58: | ||
==Allelic dominance in genetic disorders== | ==Allelic dominance in genetic disorders== | ||
A number of [[genetic disorders]] are caused when an individual inherits two recessive alleles for a single-gene trait. Recessive genetic disorders include [[albinism]], [[cystic fibrosis]], [[galactosemia]], [[phenylketonuria]] (PKU), and [[Tay–Sachs disease]]. Other disorders are also due to recessive alleles, but because the gene locus is located on the X chromosome, so that males have only one copy (that is, they are [[hemizygosity|hemizygous]]), they are more frequent in males than in females. Examples include [[Congenital red–green color blindness|red–green color blindness]] and [[fragile X syndrome]]. | A number of [[genetic disorders]] are caused when an individual inherits two recessive alleles for a single-gene trait. Recessive genetic disorders include [[albinism]], [[cystic fibrosis]], [[galactosemia]], [[phenylketonuria]] (PKU), and [[Tay–Sachs disease]].<ref>{{Cite web|title=Content - Health Encyclopedia - University of Rochester Medical Center|url=https://www.urmc.rochester.edu/encyclopedia/content?ContentTypeID=90&ContentID=P02142|website=www.urmc.rochester.edu|access-date=2025-12-01}}</ref> Other disorders are also due to recessive alleles, but because the gene locus is located on the X chromosome, so that males have only one copy (that is, they are [[hemizygosity|hemizygous]]), they are more frequent in males than in females. Examples include [[Congenital red–green color blindness|red–green color blindness]] and [[fragile X syndrome]].<ref>{{Citation|title=General aspects of X-linked diseases|url=http://www.ncbi.nlm.nih.gov/books/NBK11593/|publisher=Oxford PharmaGenesis|work=Fabry Disease: Perspectives from 5 Years of FOS|date=2006|access-date=2025-12-01|place=Oxford|isbn=978-1-903539-03-3|pmid=21290690|first=Dominique P.|last=Germain|editor-first=Atul|editor-last=Mehta|editor2-first=Michael|editor2-last=Beck|editor3-first=Gere|editor3-last=Sunder-Plassmann}}</ref> | ||
Other disorders, such as [[Huntington's disease]], occur when an individual inherits only one dominant allele. | Other disorders, such as [[Huntington's disease]], occur when an individual inherits only one dominant allele.<ref>{{Citation|title=Clinical features of early and juvenile onset in polyglutamine disorders other than Huntington's disease: autosomal dominant cerebellar ataxias and dentatorubral pallidoluysian atrophy|publisher=Oxford University Press|work=Juvenile Huntington's Disease|date=January 2009|pages=118–134|first1=André R.|last1=Troiano|first2=Alexandra|last2=Dürr |doi=10.1093/med/9780199236121.003.0008 |isbn=978-0-19-923612-1 }}</ref> | ||
==Epialleles== | ==Epialleles== | ||
While [[heredity|heritable traits]] are typically studied in terms of genetic alleles, [[epigenetic]] marks such as [[DNA methylation]] can be inherited at specific genomic regions in certain species, a process termed [[transgenerational epigenetic inheritance]]. The term ''epiallele'' is used to distinguish these heritable marks from traditional alleles, which are defined by [[nucleotide sequence]].<ref>{{cite journal|last1=Daxinger|first1=Lucia|last2=Whitelaw|first2=Emma|title=Understanding transgenerational epigenetic inheritance via the gametes in mammals|journal=Nature Reviews Genetics|date=31 January 2012|volume=13|issue=3|pages=153–62|doi=10.1038/nrg3188|pmid=22290458|s2cid=8654616}}</ref> A specific class of epiallele, the | While [[heredity|heritable traits]] are typically studied in terms of genetic alleles, [[epigenetic]] marks such as [[DNA methylation]] can be inherited at specific genomic regions in certain species, a process termed [[transgenerational epigenetic inheritance]]. The term ''epiallele'' is used to distinguish these heritable marks from traditional alleles, which are defined by [[nucleotide sequence]].<ref>{{cite journal|last1=Daxinger|first1=Lucia|last2=Whitelaw|first2=Emma|title=Understanding transgenerational epigenetic inheritance via the gametes in mammals|journal=Nature Reviews Genetics|date=31 January 2012|volume=13|issue=3|pages=153–62|doi=10.1038/nrg3188|pmid=22290458|s2cid=8654616}}</ref> A specific class of epiallele, the metastable epialleles, has been discovered in mice and in humans which is characterized by stochastic (probabilistic) establishment of epigenetic state that can be mitotically inherited.<ref>{{cite journal|last1=Rakyan|first1=Vardhman K|last2=Blewitt|first2=Marnie E|last3=Druker|first3=Riki|last4=Preis|first4=Jost I|last5=Whitelaw|first5=Emma|title=Metastable epialleles in mammals|journal=Trends in Genetics|date=July 2002|volume=18|issue=7|pages=348–351|doi=10.1016/S0168-9525(02)02709-9|pmid=12127774}}</ref><ref>{{cite journal|last1=Waterland|first1=RA|last2=Dolinoy|first2=DC|last3=Lin|first3=JR|last4=Smith|first4=CA|last5=Shi|first5=X|last6=Tahiliani|first6=KG|title=Maternal methyl supplements increase offspring DNA methylation at Axin Fused.|journal=Genesis|date=September 2006|volume=44|issue=9|pages=401–6|pmid=16868943|doi=10.1002/dvg.20230|s2cid=36938621}}</ref> | ||
==Idiomorph== | ==Idiomorph== | ||
The term "idiomorph", from Greek 'morphos' (form) and 'idio' (singular, unique), was introduced in 1990 in place of "allele" to denote sequences at the same locus in different strains that have no sequence similarity and probably do not share a common phylogenetic relationship. It is used mainly in the genetic research of [[mycology]].<ref>{{Cite journal |doi=10.1093/genetics/132.1.125 |doi-access=free |pmc=1205111 |pmid=1398049|title=Isolation of Neurospora crassa a mating type mutants by repeat induced point (RIP) mutation |year=1992 |last1=Glass |first1=N. L. |last2=Lee |first2=L. |journal=Genetics |volume=132 |pages=125–133 }}</ref><ref>{{Cite journal |doi=10.1002/bies.950120202|title=Mating type and mating strategies in ''Neurospora'' |year=1990 |last1=Metzenberg |first1=Robert L. |last2=Glass |first2=N. Louise |journal=BioEssays |volume=12 |issue=2 |pages=53–59 |pmid=2140508 |s2cid=10818930 }}</ref> | The term "idiomorph", from Greek 'morphos' (form) and 'idio' (singular, unique), was introduced in 1990 in place of "allele" to denote sequences at the same locus in different strains that have no sequence similarity and probably do not share a common phylogenetic relationship. It is used mainly in the genetic research of [[mycology]].<ref>{{Cite journal |doi=10.1093/genetics/132.1.125 |doi-access=free |pmc=1205111 |pmid=1398049|title=Isolation of Neurospora crassa a mating type mutants by repeat induced point (RIP) mutation |year=1992 |last1=Glass |first1=N. L. |last2=Lee |first2=L. |journal=Genetics |volume=132 |pages=125–133 }}</ref><ref>{{Cite journal |doi=10.1002/bies.950120202|title=Mating type and mating strategies in ''Neurospora'' |year=1990 |last1=Metzenberg |first1=Robert L. |last2=Glass |first2=N. Louise |journal=BioEssays |volume=12 |issue=2 |pages=53–59 |pmid=2140508 |bibcode=1990BiEss..12...53M |s2cid=10818930 }}</ref> | ||
==See also== | ==See also== | ||
{{Portal|Evolutionary biology}} | {{Portal|Evolutionary biology}} | ||
{{Wiktionary|allele}} | |||
{{Columns-list|colwidth=22em| | {{Columns-list|colwidth=22em| | ||
* [[Allelotype]] | * [[Allelotype]] | ||
| Line 89: | Line 89: | ||
==References and notes== | ==References and notes== | ||
{{Reflist|refs=<ref name="OnlineMendelianInheritanceinMan">{{cite web|url=https://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=110300 |title=ABO Glycosyltransferase; ABO |author1=Victor A. McKusick |author2=Cassandra L. Kniffin |author3=Paul J. Converse |author4=Ada Hamosh |date=10 November 2009 |work=Online Mendelian Inheritance in Man |publisher=National Library of Medicine |access-date=24 March 2010 |archive-url=https://web.archive.org/web/20080924220935/http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=110300 |archive-date=24 September 2008 | {{Reflist|refs=<ref name="OnlineMendelianInheritanceinMan">{{cite web|url=https://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=110300 |title=ABO Glycosyltransferase; ABO |author1=Victor A. McKusick |author2=Cassandra L. Kniffin |author3=Paul J. Converse |author4=Ada Hamosh |date=10 November 2009 |work=Online Mendelian Inheritance in Man |publisher=National Library of Medicine |access-date=24 March 2010 |archive-url=https://web.archive.org/web/20080924220935/http://www.ncbi.nlm.nih.gov/entrez/dispomim.cgi?id=110300 |archive-date=24 September 2008 }}</ref><ref name="Essential genetics: A genomics perspective">{{cite book |title=Essential genetics: A genomics perspective |edition=4th |last=Hartl |first=Daniel L. |author2=Elizabeth W. Jones |year=2005 |publisher=Jones & Bartlett Publishers |isbn=978-0-7637-3527-2 |page=600 }}<!--|access-date=5 October 2009--></ref><ref name="Sequence variation at the human ABO locus">{{cite journal |author=Yip SP |title=Sequence variation at the human ABO locus |journal=Annals of Human Genetics |volume=66 |issue=1 |pages=1–27 |date=January 2002 |pmid=12014997 |doi=10.1017/S0003480001008995|doi-access=free }}</ref> | ||
}} | }} | ||
== | * {{Cite journal|title=What can we learn from selfish loci that break Mendel's law?|journal=PLOS Biology|date=2022-07-19|issn=1545-7885|pmc=9295977|pmid=35853012|article-number=e3001700|volume=20|issue=7|doi=10.1371/journal.pbio.3001700|language=en|first=Sarah E.|last=Zanders | doi-access=free }} | ||
{{Genetics}} | {{Genetics}} | ||
{{Authority control}} | {{Authority control}} | ||
[[Category:Classical genetics]] | [[Category:Classical genetics]] | ||
[[Category:Genetic genealogy]] | [[Category:Genetic genealogy]] | ||