Dominance (genetics)

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Autosomal dominant and autosomal recessive inheritance, the two most common Mendelian inheritance patterns. An autosome is any chromosome other than a sex chromosome. Autosomal dominant and recessive.svg
Autosomal dominant and autosomal recessive inheritance, the two most common Mendelian inheritance patterns. An autosome is any chromosome other than a sex chromosome.

In genetics, dominance is the phenomenon of one variant (allele) of a gene on a chromosome masking or overriding the effect of a different variant of the same gene on the other copy of the chromosome. [1] [2] The first variant is termed dominant and the second is called recessive. This state of having two different variants of the same gene on each chromosome is originally caused by a mutation in one of the genes, either new (de novo) or inherited. The terms autosomal dominant or autosomal recessive are used to describe gene variants on non-sex chromosomes (autosomes) and their associated traits, while those on sex chromosomes (allosomes) are termed X-linked dominant, X-linked recessive or Y-linked; these have an inheritance and presentation pattern that depends on the sex of both the parent and the child (see Sex linkage). Since there is only one copy of the Y chromosome, Y-linked traits cannot be dominant or recessive. [3] Additionally, there are other forms of dominance, such as incomplete dominance, in which a gene variant has a partial effect compared to when it is present on both chromosomes, and co-dominance, in which different variants on each chromosome both show their associated traits.

Contents

Dominance is a key concept in Mendelian inheritance and classical genetics. Letters and Punnett squares are used to demonstrate the principles of dominance in teaching, and the upper-case letters are used to denote dominant alleles and lower-case letters are used for recessive alleles. An often quoted example of dominance is the inheritance of seed shape in peas. Peas may be round, associated with allele R, or wrinkled, associated with allele r. In this case, three combinations of alleles (genotypes) are possible: RR, Rr, and rr. The RR (homozygous) individuals have round peas, and the rr (homozygous) individuals have wrinkled peas. In Rr (heterozygous) individuals, the R allele masks the presence of the r allele, so these individuals also have round peas. Thus, allele R is dominant over allele r, and allele r is recessive to allele R. [4]

Dominance is not inherent to an allele or its traits (phenotype). It is a strictly relative effect between two alleles of a given gene of any function; one allele can be dominant over a second allele of the same gene, recessive to a third, and co-dominant with a fourth. Additionally, one allele may be dominant for one trait but not others. [5] Dominance differs from epistasis, the phenomenon of an allele of one gene masking the effect of alleles of a different gene. [6]

Background

Inheritance of dwarfing in maize. Demonstrating the heights of plants from the two parent variations and their F1 heterozygous hybrid (centre) Journal of Agricultural Research (1917) (14582377398).jpg
Inheritance of dwarfing in maize. Demonstrating the heights of plants from the two parent variations and their F1 heterozygous hybrid (centre)

Gregor Johann Mendel, "The Father of Genetics", promulgated the idea of dominance in the 1860s. However, it was not widely known until the early twentieth century. Mendel observed that, for a variety of traits of garden peas having to do with the appearance of seeds, seed pods, and plants, there were two discrete phenotypes, such as round versus wrinkled seeds, yellow versus green seeds, red versus white flowers or tall versus short plants. When bred separately, the plants always produced the same phenotypes, generation after generation. However, when lines with different phenotypes were crossed (interbred), one and only one of the parental phenotypes showed up in the offspring (green, round, red, or tall). However, when these hybrid plants were crossed, the offspring plants showed the two original phenotypes, in a characteristic 3:1 ratio, the more common phenotype being that of the parental hybrid plants. Mendel reasoned that each parent in the first cross was a homozygote for different alleles (one parent AA and the other parent aa), that each contributed one allele to the offspring, with the result that all of these hybrids were heterozygotes (Aa), and that one of the two alleles in the hybrid cross dominated expression of the other: A masked a. The final cross between two heterozygotes (Aa X Aa) would produce AA, Aa, and aa offspring in a 1:2:1 genotype ratio with the first two classes showing the (A) phenotype, and the last showing the (a) phenotype, thereby producing the 3:1 phenotype ratio.

Mendel did not use the terms gene, allele, phenotype, genotype, homozygote, and heterozygote, all of which were introduced later. He did introduce the notation of capital and lowercase letters for dominant and recessive alleles, respectively, still in use today.

In 1928, British population geneticist Ronald Fisher proposed that dominance acted based on natural selection through the contribution of modifier genes. In 1929, American geneticist Sewall Wright responded by stating that dominance is simply a physiological consequence of metabolic pathways and the relative necessity of the gene involved. [7] [8] [9] [5]

Types of dominance

Complete dominance (Mendelian)

In complete dominance, the effect of one allele in a heterozygous genotype completely masks the effect of the other. The allele that masks are considered dominant to the other allele, and the masked allele is considered recessive. [10]

When we only look at one trait determined by one pair of genes, we call it monohybrid inheritance . If the crossing is done between parents (P-generation, F0-generation) who are homozygote dominant and homozygote recessive, the offspring (F1-generation) will always have the heterozygote genotype and always present the phenotype associated with the dominant gene.

Monohybrid cross between homozygote dominant (GG) and homozygote recessive (gg), always resulting in heterozygote genotype (Gg) and the phenotype associated with the dominant allele, in this case capital G. MonohydrideP.png
Monohybrid cross between homozygote dominant (GG) and homozygote recessive (gg), always resulting in heterozygote genotype (Gg) and the phenotype associated with the dominant allele, in this case capital G.
Monohybrid cross between heterozygotes (Gg), resulting in genptypical ratio 1:2:1 (GG:Gg:gg) and phenotypical ratio 3:1 (G:g). MonohydrideF1.png
Monohybrid cross between heterozygotes (Gg), resulting in genptypical ratio 1:2:1 (GG:Gg:gg) and phenotypical ratio 3:1 (G:g).

However, if the F1-generation is further crossed with the F1-generation (heterozygote crossed with heterozygote) the offspring (F2-generation) will present the phenotype associated with the dominant gene ¾ times. Although heterozygote monohybrid crossing can result in two phenotype variants, it can result in three genotype variants -  homozygote dominant, heterozygote and homozygote recessive, respectively. [11]

In dihybrid inheritance we look at the inheritance of two pairs of genes simultaneous. Assuming here that the two pairs of genes are located at non-homologous chromosomes, such that they are not coupled genes (see genetic linkage) but instead inherited independently. Consider now the cross between parents (P-generation) of genotypes homozygote dominant and recessive, respectively. The offspring (F1-generation) will always heterozygous and present the phenotype associated with the dominant allele variant.

Dihybrid cross between homozygote dominant (GGRR) and homozygote recessive (ggrr) always resulting in heterozygotes (GgRr) with phenotype associated with the dominant alleles G and R. DihydrideP.png
Dihybrid cross between homozygote dominant (GGRR) and homozygote recessive (ggrr) always resulting in heterozygotes (GgRr) with phenotype associated with the dominant alleles G and R.
Dihybrid cross between heterozygotes (GgRr), resulting in the phenotypical ratio 9:3:3:1 (G and R: G and r: g and R: g and r) DihydrideF1.png
Dihybrid cross between heterozygotes (GgRr), resulting in the phenotypical ratio 9:3:3:1 (G and R: G and r: g and R: g and r)

However, when crossing the F1-generation there are four possible phenotypic possibilities and the phenotypical ratio for the F2-generation will always be 9:3:3:1. [12]

Incomplete dominance (non-Mendelian)

This Punnett square illustrates incomplete dominance. In this example, the red petal trait associated with the R allele recombines with the white petal trait of the r allele. The plant incompletely expresses the dominant trait (R) causing plants with the Rr genotype to express flowers with less red pigment resulting in pink flowers. The colors are not blended together, the dominant trait is just expressed less strongly. Incomplete dominance.svg
This Punnett square illustrates incomplete dominance. In this example, the red petal trait associated with the R allele recombines with the white petal trait of the r allele. The plant incompletely expresses the dominant trait (R) causing plants with the Rr genotype to express flowers with less red pigment resulting in pink flowers. The colors are not blended together, the dominant trait is just expressed less strongly.

Incomplete dominance (also called partial dominance, semi-dominance, intermediate inheritance, or occasionally incorrectly co-dominance in reptile genetics [13] ) occurs when the phenotype of the heterozygous genotype is distinct from and often intermediate to the phenotypes of the homozygous genotypes. The phenotypic result often appears as a blended form of characteristics in the heterozygous state. For example, the snapdragon flower color is homozygous for either red or white. When the red homozygous flower is paired with the white homozygous flower, the result yields a pink snapdragon flower. The pink snapdragon is the result of incomplete dominance. A similar type of incomplete dominance is found in the four o'clock plant wherein pink color is produced when true-bred parents of white and red flowers are crossed. In quantitative genetics, where phenotypes are measured and treated numerically, if a heterozygote's phenotype is exactly between (numerically) that of the two homozygotes, the phenotype is said to exhibit no dominance at all, i.e. dominance exists only when the heterozygote's phenotype measure lies closer to one homozygote than the other.

When plants of the F1 generation are self-pollinated, the phenotypic and genotypic ratio of the F2 generation will be 1:2:1 (Red:Pink:White). [14]

Co-dominance (non-Mendelian)

Co-dominance in a Camellia cultivar Co-dominance Rhododendron.jpg
Co-dominance in a Camellia cultivar
A and B blood types in humans show co-dominance, but the O type is recessive to A and B. ABO system codominance.svg
A and B blood types in humans show co-dominance, but the O type is recessive to A and B.
This Punnett square shows co-dominance. In this example a white bull (WW) mates with a red cow (RR), and their offspring exhibit co-dominance expressing both white and red hairs. Co-dominance in Roan Cattle.svg
This Punnett square shows co-dominance. In this example a white bull (WW) mates with a red cow (RR), and their offspring exhibit co-dominance expressing both white and red hairs.

Co-dominance occurs when the contributions of both alleles are visible in the phenotype and neither allele masks another.

For example, in the ABO blood group system, chemical modifications to a glycoprotein (the H antigen) on the surfaces of blood cells are controlled by three alleles, two of which are co-dominant to each other (IA, IB) and dominant over the recessive i at the ABO locus. The IA and IB alleles produce different modifications. The enzyme coded for by IA adds an N-acetylgalactosamine to a membrane-bound H antigen. The IB enzyme adds a galactose. The i allele produces no modification. Thus the IA and IB alleles are each dominant to i (IAIA and IAi individuals both have type A blood, and IBIB and IBi individuals both have type B blood), but IAIB individuals have both modifications on their blood cells and thus have type AB blood, so the IA and IB alleles are said to be co-dominant. [14]

Another example occurs at the locus for the beta-globin component of hemoglobin, where the three molecular phenotypes of HbA/HbA, HbA/HbS, and HbS/HbS are all distinguishable by protein electrophoresis. (The medical condition produced by the heterozygous genotype is called sickle-cell trait and is a milder condition distinguishable from sickle-cell anemia , thus the alleles show incomplete dominance concerning anemia, see above). For most gene loci at the molecular level, both alleles are expressed co-dominantly, because both are transcribed into RNA. [14]

Co-dominance, where allelic products co-exist in the phenotype, is different from incomplete dominance, where the quantitative interaction of allele products produces an intermediate phenotype. For example, in co-dominance, a red homozygous flower and a white homozygous flower will produce offspring that have red and white spots. When plants of the F1 generation are self-pollinated, the phenotypic and genotypic ratio of the F2 generation will be 1:2:1 (Red:Spotted:White). These ratios are the same as those for incomplete dominance. Again, this classical terminology is inappropriate – in reality, such cases should not be said to exhibit dominance at all. [14]

Relationship to other genetic concepts

Dominance can be influenced by various genetic interactions and it is essential to evaluate them when determining phenotypic outcomes. Multiple alleles, epistasis and pleiotropic genes are some factors that might influence the phenotypic outcome. [15]

Multiple alleles

Although any individual of a diploid organism has at most two different alleles at a given locus, most genes exist in a large number of allelic versions in the population as a whole. This is called polymorphism, and is caused by mutations. Polymorphism can have an effect on the dominance relationship and phenotype, which is observed in the ABO blood group system. The gene responsible for human blood type have three alleles; A, B, and O, and their interactions result in different blood types based on the level of dominance the alleles expresses towards each other. [15] [16]

Pleiotropic genes

Pleiotropic genes are genes where one single gene affects two or more characters (phenotype). This means that a gene can have a dominant effect on one trait, but a more recessive effect on another trait. [17]

Epistasis

Epistasis is interactions between multiple alleles at different loci. Easily said, several genes for one phenotype. The dominance relationship between alleles involved in epistatic interactions can influence the observed phenotypic ratios in offspring. [18]

See also

Related Research Articles

An allele, or allelomorph, is a variant of the sequence of nucleotides at a particular location, or locus, on a DNA molecule.

The genotype of an organism is its complete set of genetic material. Genotype can also be used to refer to the alleles or variants an individual carries in a particular gene or genetic location. The number of alleles an individual can have in a specific gene depends on the number of copies of each chromosome found in that species, also referred to as ploidy. In diploid species like humans, two full sets of chromosomes are present, meaning each individual has two alleles for any given gene. If both alleles are the same, the genotype is referred to as homozygous. If the alleles are different, the genotype is referred to as heterozygous.

<span class="mw-page-title-main">Mendelian inheritance</span> Type of biological inheritance

Mendelian inheritance is a type of biological inheritance following the principles originally proposed by Gregor Mendel in 1865 and 1866, re-discovered in 1900 by Hugo de Vries and Carl Correns, and later popularized by William Bateson. These principles were initially controversial. When Mendel's theories were integrated with the Boveri–Sutton chromosome theory of inheritance by Thomas Hunt Morgan in 1915, they became the core of classical genetics. Ronald Fisher combined these ideas with the theory of natural selection in his 1930 book The Genetical Theory of Natural Selection, putting evolution onto a mathematical footing and forming the basis for population genetics within the modern evolutionary synthesis.

<span class="mw-page-title-main">Punnett square</span> Tabular summary of genetic combinations

The Punnett square is a square diagram that is used to predict the genotypes of a particular cross or breeding experiment. It is named after Reginald C. Punnett, who devised the approach in 1905. The diagram is used by biologists to determine the probability of an offspring having a particular genotype. The Punnett square is a tabular summary of possible combinations of maternal alleles with paternal alleles. These tables can be used to examine the genotypical outcome probabilities of the offspring of a single trait (allele), or when crossing multiple traits from the parents. The Punnett square is a visual representation of Mendelian inheritance, a fundamental concept in genetics which is discovery of Gregor Mendel. For multiple traits, using the "forked-line method" is typically much easier than the Punnett square. Phenotypes may be predicted with at least better-than-chance accuracy using a Punnett square, but the phenotype that may appear in the presence of a given genotype can in some instances be influenced by many other factors, as when polygenic inheritance and/or epigenetics are at work.

Balancing selection refers to a number of selective processes by which multiple alleles are actively maintained in the gene pool of a population at frequencies larger than expected from genetic drift alone. Balancing selection is rare compared to purifying selection. It can occur by various mechanisms, in particular, when the heterozygotes for the alleles under consideration have a higher fitness than the homozygote. In this way genetic polymorphism is conserved.

A heterozygote advantage describes the case in which the heterozygous genotype has a higher relative fitness than either the homozygous dominant or homozygous recessive genotype. Loci exhibiting heterozygote advantage are a small minority of loci. The specific case of heterozygote advantage due to a single locus is known as overdominance. Overdominance is a rare condition in genetics where the phenotype of the heterozygote lies outside of the phenotypical range of both homozygote parents, and heterozygous individuals have a higher fitness than homozygous individuals.

<span class="mw-page-title-main">Overdominance</span>

Overdominance is a phenomenon in genetics where the phenotype of the heterozygote lies outside the phenotypical range of both homozygous parents. Overdominance can also be described as heterozygote advantage regulated by a single genomic locus, wherein heterozygous individuals have a higher fitness than homozygous individuals. However, not all cases of the heterozygote advantage are considered overdominance, as they may be regulated by multiple genomic regions. Overdominance has been hypothesized as an underlying cause for heterosis.

<span class="mw-page-title-main">Equine coat color genetics</span> Genetics behind the equine coat color

Equine coat color genetics determine a horse's coat color. Many colors are possible, but all variations are produced by changes in only a few genes. Bay is the most common color of horse, followed by black and chestnut. A change at the agouti locus is capable of turning bay to black, while a mutation at the extension locus can turn bay or black to chestnut.

<span class="mw-page-title-main">Monohybrid cross</span> Cross between two organisms with different variations at one genetic locus of interest

A monohybrid cross is a cross between two organisms with different variations at one genetic locus of interest. The character(s) being studied in a monohybrid cross are governed by two or multiple variations for a single location of a gene. Then carry out such a cross, each parent is chosen to be homozygous or true breeding for a given trait (locus). When a cross satisfies the conditions for a monohybrid cross, it is usually detected by a characteristic distribution of second-generation (F2) offspring that is sometimes called the monohybrid ratio.

<span class="mw-page-title-main">Non-Mendelian inheritance</span> Type of pattern of inheritance

Non-Mendelian inheritance is any pattern in which traits do not segregate in accordance with Mendel's laws. These laws describe the inheritance of traits linked to single genes on chromosomes in the nucleus. In Mendelian inheritance, each parent contributes one of two possible alleles for a trait. If the genotypes of both parents in a genetic cross are known, Mendel's laws can be used to determine the distribution of phenotypes expected for the population of offspring. There are several situations in which the proportions of phenotypes observed in the progeny do not match the predicted values.

Dihybrid cross is a cross between two individuals with two observed traits that are controlled by two distinct genes. The idea of a dihybrid cross came from Gregor Mendel when he observed pea plants that were either yellow or green and either round or wrinkled. Crossing of two heterozygous individuals will result in predictable ratios for both genotype and phenotype in the offspring. The expected phenotypic ratio of crossing heterozygous parents would be 9:3:3:1. Deviations from these expected ratios may indicate that the two traits are linked or that one or both traits has a non-Mendelian mode of inheritance.

Inbreeding depression is the reduced biological fitness that has the potential to result from inbreeding. The loss of genetic diversity that is seen due to inbreeding, results from small population size. Biological fitness refers to an organism's ability to survive and perpetuate its genetic material. Inbreeding depression is often the result of a population bottleneck. In general, the higher the genetic variation or gene pool within a breeding population, the less likely it is to suffer from inbreeding depression, though inbreeding and outbreeding depression can simultaneously occur.

<span class="mw-page-title-main">Test cross</span>

Under the law of dominance in genetics, an individual expressing a dominant phenotype could contain either two copies of the dominant allele or one copy of each dominant and recessive allele. By performing a test cross, one can determine whether the individual is heterozygous or homozygous dominant.

Balancer chromosomes are a type of genetically engineered chromosome used in laboratory biology for the maintenance of recessive lethal mutations within living organisms without interference from natural selection. Since such mutations are viable only in heterozygotes, they cannot be stably maintained through successive generations and therefore continually lead to production of wild-type organisms, which can be prevented by replacing the homologous wild-type chromosome with a balancer. In this capacity, balancers are crucial for genetics research on model organisms such as Drosophila melanogaster, the common fruit fly, for which stocks cannot be archived. They can also be used in forward genetics screens to specifically identify recessive lethal mutations. For that reason, balancers are also used in other model organisms, most notably the nematode worm Caenorhabditis elegans and the mouse.

In medical genetics, compound heterozygosity is the condition of having two or more heterogeneous recessive alleles at a particular locus that can cause genetic disease in a heterozygous state; that is, an organism is a compound heterozygote when it has two recessive alleles for the same gene, but with those two alleles being different from each other. Compound heterozygosity reflects the diversity of the mutation base for many autosomal recessive genetic disorders; mutations in most disease-causing genes have arisen many times. This means that many cases of disease arise in individuals who have two unrelated alleles, who technically are heterozygotes, but both the alleles are defective.

Lethal alleles are alleles that cause the death of the organism that carries them. They are usually a result of mutations in genes that are essential for growth or development. Lethal alleles may be recessive, dominant, or conditional depending on the gene or genes involved.

<span class="mw-page-title-main">Hereditary carrier</span> Organism with a recessive genetic allele that does not display the recessive trait

A hereditary carrier, is a person or other organism that has inherited a recessive allele for a genetic trait or mutation but usually does not display that trait or show symptoms of the disease. Carriers are, however, able to pass the allele onto their offspring, who may then express the genetic trait.

<span class="mw-page-title-main">Zygosity</span> Degree of similarity of the alleles in an organism

Zygosity is the degree to which both copies of a chromosome or gene have the same genetic sequence. In other words, it is the degree of similarity of the alleles in an organism.

Classical genetics is the branch of genetics based solely on visible results of reproductive acts. It is the oldest discipline in the field of genetics, going back to the experiments on Mendelian inheritance by Gregor Mendel who made it possible to identify the basic mechanisms of heredity. Subsequently, these mechanisms have been studied and explained at the molecular level.

This glossary of genetics and evolutionary biology is a list of definitions of terms and concepts used in the study of genetics and evolutionary biology, as well as sub-disciplines and related fields, with an emphasis on classical genetics, quantitative genetics, population biology, phylogenetics, speciation, and systematics. Overlapping and related terms can be found in Glossary of cellular and molecular biology, Glossary of ecology, and Glossary of biology.

References

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  2. ↑ "express". Oxford Dictionaries Online. Oxford University Press. Archived from the original on July 18, 2012. Retrieved 14 May 2014.
  3. ↑ Eggers, Stefanie; Sinclair, Andrew (2012). "Mammalian sex determination—insights from humans and mice". Chromosome Res. 20 (1). Dordrecht: Springer-Verlag: 215–238. doi:10.1007/s10577-012-9274-3. hdl: 11343/270255 . ISSN   0967-3849. PMID   22290220.
  4. ↑ Bateson, William; Mendel, Gregor (2009). Mendel's Principles of Heredity: A Defence, with a Translation of Mendel's Original Papers on Hybridisation. Cambridge University Press. doi:10.1017/CBO9780511694462. ISBN   978-1108006132.
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  6. ↑ Griffiths AJF; Gelbart WM; Miller JH; et al. (1999). "Gene Interaction Leads to Modified Dihybrid Ratios". Modern Genetic Analysis . New York: W. H. Freeman & Company. ISBN   978-0-7167-3118-4.
  7. ↑ Mayo, O. and Bürger, R. 1997. The evolution of dominance: A theory whose time has passed? Archived 2016-03-04 at the Wayback Machine "Biological Reviews", Volume 72, Issue 1, pp. 97–110
  8. ↑ Bourguet, D. 1999. The evolution of dominance Archived 2016-08-29 at the Wayback Machine Heredity, Volume 83, Number 1, pp. 1–4
  9. ↑ Bagheri, H.C. 2006. Unresolved boundaries of evolutionary theory and the question of how inheritance systems evolve: 75 years of debate on the evolution of dominance Archived 2019-07-02 at the Wayback Machine "Journal of Experimental Zoology Part B: Molecular and Developmental Evolution", Volume 306B, Issue 4, pp. 329–359
  10. ↑ Rodríguez-Beltrán, Jerónimo; Sørum, Vidar; Toll-Riera, Macarena; de la Vega, Carmen; Peña-Miller, Rafael; San Millán, Álvaro (2020). "Genetic dominance governs the evolution and spread of mobile genetic elements in bacteria". Proc Natl Acad Sci U S A. 117 (27). United States: United States: National Academy of Sciences: 15755–15762. Bibcode:2020PNAS..11715755R. doi: 10.1073/pnas.2001240117 . ISSN   0027-8424. PMC   7355013 . PMID   32571917.
  11. ↑ Trudy, F. C. Mackay; Robert, R. H. Anholt (2022). "Gregor Mendel's legacy in quantitative genetics". PLOS Biology. 20 (7). Public Library of Science (PLoS): e3001692. doi: 10.1371/journal.pbio.3001692 . ISSN   1544-9173. PMC   9295954 . PMID   35852997.
  12. ↑ Alberts, Bruce; Heald, Rebecca; Hopkin, Karen; Johnson, Alexander; Morgan, David; Roberts, Keith; Walter, Peter (2023). Essential cell biology (Sixth edition.; International student ed.). W.W. Norton & Company. ISBN   9781324033394.
  13. ↑ Bulinski, Steven (2016-01-05). "A Crash Course in Reptile Genetics". Reptiles . Living World Media. Archived from the original on 2020-02-04. Retrieved 2023-02-03. The term co-dominant is often used interchangeably with incomplete dominant, but the two terms have different meanings.
  14. 1 2 3 4 Brown, T. A. (2018). Genomes 4 (4th ed.). Milton: Milton: Garland Science. doi:10.1201/9781315226828. ISBN   9780815345084. S2CID   239528980.
  15. 1 2 Ingelman-Sundberg, M. (2005). "Genetic polymorphisms of cytochrome P450 2D6 (CYP2D6): clinical consequences, evolutionary aspects and functional diversity". Pharmacogenomics J. 5 (1). United States: United States: Nature Publishing Group: 6–13. doi:10.1038/sj.tpj.6500285. ISSN   1470-269X. PMID   15492763. S2CID   10695794.
  16. ↑ Yamamoto, F; Clausen, H; White, T; Marken, J; Hakomori, S (1990). "Molecular genetic basis of the histo-blood group ABO system". Nature. 345 (6272): 229–233. Bibcode:1990Natur.345..229Y. doi:10.1038/345229a0. PMID   2333095. S2CID   4237562.
  17. ↑ Du, Qingzhang; Tian, Jiaxing; Yang, Xiaohui; Pan, Wei; Xu, Baohua; Li, Bailian; Ingvarsson, Pär K.; Zhang, Deqiang (2015). "Identification of additive, dominant, and epistatic variation conferred by key genes in cellulose biosynthesis pathway in Populus tomentosa". DNA Res. 22 (1). England: England: Oxford University Press: 53–67. doi:10.1093/dnares/dsu040. ISSN   1340-2838. PMC   4379978 . PMID   25428896.
  18. ↑ Phillips, Patrick C (2008). "Epistasis - the essential role of gene interactions in the structure and evolution of genetic systems". Nat Rev Genet. 9 (11). London: London: Nature Publishing Group: 855–867. doi:10.1038/nrg2452. ISSN   1471-0056. PMC   2689140 . PMID   18852697.
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