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How Incomplete dominance can be explained at molecular level?

How Incomplete dominance can be explained at molecular level?


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What is exactly happening at the molecular level when two alleles constitute incomplete dominance? Whether the protein formed from each of the alleles constitute a new protein having a different function or anything happens at the RNA level of the two alleles.


Molecular mechanisms of incomplete dominance (a.k.a. partial- or semi-dominance) vary. As an example, let's look at snapdragons and morning glories, two flowering plants that both exhibit incomplete dominance relative to flower pigmentation.

Snapdragons (Antirrhinum majus) have multiple alleles at the nivea locus. The wild-type nivea transcript (niv+) encodes a chalcone synthase involved in pigment biosynthesis, and a single copy of the niv+ allele is sufficient for wild-type pigmentation. However, niv+ is semi-dominant with the mutant niv-525 allele, leading to reduced pigmentation in the heterozygote. The original publication by Coen and Carpenter 1 describing this effect offers some possible molecular explanations:

  1. Transcription factor sequestration. The niv-525 allele could encode a defective enzyme. This allele also contains an inverted duplication of a transcription factor binding domain required for enzyme expression. The defective niv-525 allele therefore titrates away transcription factor from niv+, leading to less enzyme and therefore less pigment.

  2. Transvection. There is some physical interaction between alleles on homologous chromosomes, such that transcription of one or both alleles is activated or repressed in trans. This could be realized as binding of the enhancer associated with the wild-type allele to the promoter of the defective allele. Figure 9 of Gohl et al. 2 has a good explanatory graphic.

  3. Anti-sense hybridization. The inverted duplication on the niv-525 allele contains a TATA box. Transcription initiated at this site would result in a transcript anti-sense to the wild-type mRNA. Hybridization of the sense and anti-sense RNAs creates dsRNA that is selectively degraded and/or inefficiently transported out of the nucleus, ultimately leading to less enzyme product.

Morning glories (Ipomoea purpurea) show similar genetics at the A locus, which also encodes a chalcone synthase. However, unlike the snapdragon niv+ allele, a single copy of the wild-type a allele is not sufficient to produce wild-type pigmentation. Therefore, incomplete dominance in morning glory results from a simple dosage-dependent mechanism, as described in Johzuka-Hisatomi et al. 3

Citations

  1. Coen ES, Carpenter R. A semi-dominant allele, niv-525, acts in trans to inhibit expression of its wild-type homologue in Antirrhinum majus. EMBO J. 1988;7(4):877-883.
  2. Gohl D, Müller M, Pirrotta V, Affolter M, Schedl P. Enhancer blocking and transvection at the Drosophila apterous locus. Genetics. 2008;178(1):127-143.
  3. Johzuka-Hisatomi Y, Noguchi H, Iida S. The molecular basis of incomplete dominance at the A locus of CHS-D in the common morning glory, Ipomoea purpurea. J Plant Res. 2011;124(2):299-304.

Strictly speaking, incomplete dominance is an interaction between two alleles of the same gene not between two genes.

The most common cause of this is the dosage effect. For example, the product of CHS-D gene is an enzyme required for the synthesis of purple pigment anthocyanin in morning glory flowers. If a plant has two functional (A) alleles of this gene it produces enough pigment to have intensely purple flowers. The a allele has the loss-of-function mutation (isn't able to produce working enzyme) so homozygous a/a plants will lack purple pigment resulting in white flowers. But heterozygous A/a plants have half of the normal enzyme level and half of the pigment so the flowers are lighter purple (source). Genes like this are said to be haploinsufficient. In cases of full dominance, one functional copy of the gene is enough to produce a "normal" phenotype (the gene is haplosufficient) or the gene is upregulated to bring the concentration of functional products to the required level (source).

There are other mechanisms for incomplete dominance. For example, in snapdragon flowers, the allele niv-571 at nivea locus can inhibit the expression of "normal" Niv+ allele in heterozygous plants (source).


Dominance or Recessiveness is the characteristic of allele, not gene.

Particular gene contains data for producing specific protein. Protein produced from one allele can effect protein synthesis of other one. Protein formed from recessive allele can show dominance over the dominant allele, and this is known as Dominant negative.

The protein produced from one allele is faulty and prevents other allele's protein to work properly. Both the proteins interact with each other in particular cell.

Genetic trait for red hair is an example of dominant negative. Gene MC1R is responsible for red hair. Protein produced by this gene converts red pigment into brown. When this protein is faulty the red pigment is accumulated and hair appears red in colour. Usually red hair is recessive trait. Two faulty MC1R gene results in read hair characteristic. Both the proteins formed from MC1R gene need to bind so that red pigment converts into brown. But when functioning product binds with faulty one, the protein becomes defective. So this defective MC1R protein is responsible for showing dominance.

https://genetics.thetech.org/ask-a-geneticist/genotype-vs-phenotype


What is Incomplete Dominance? (With Examples)

The incomplete dominance it is the genetic phenomenon in which the dominant allele does not mask the effect of the recessive allele completely that is, it is not completely dominant. It is also known as semi-dominance, a name that clearly describes what happens in alleles.

Before its discovery, what had been observed was the complete dominance of the characters in the offspring. The incomplete dominance was described for the first time in 1905 by the German botanist Carl Correns, in his studies of the color of the flowers of the species Mirabilis jalapa.

Intermediate phenotype in F1 generation caused by incomplete dominance

The effect of incomplete dominance becomes evident when the heterozygous descendants of a cross between homozygotes are observed.

In this case, the descendants have an intermediate phenotype to that of the parents and not the dominant phenotype, which is what is observed in cases where dominance is complete.

In genetics, dominance refers to the property of a gene (or allele) in relation to other genes or alleles. An allele shows dominance when it suppresses the expression or dominates the effects of the recessive allele. There are several forms of dominance: complete dominance, incomplete dominance and codominance.

In incomplete dominance, the aspect of the descendants is the result of the partial influence of both alleles or genes. Incomplete dominance occurs in the polygenic inheritance (many genes) of traits such as the color of eyes, flowers and skin.

  • 1 Examples
    • 1.1 The flowers of the Correns experiment (Mirabilis jalapa)
    • 1.2 Peas from Mendel's experiment (Pisum sativum)
    • 1.3 The enzyme hexosaminidase A (Hex-A)
    • 1.4 Familial hypercholesterolemia

    Complete Dominance

    Ion-Bogdan DUMITRESCU/Moment/Getty Images

    In complete dominance relationships, one allele is dominant and the other is recessive. The dominant allele for a trait completely masks the recessive allele for that trait. The phenotype is determined by the dominant allele. For example, the genes for seed shape in pea plants exists in two forms, one form or allele for round seed shape (R) and the other for wrinkled seed shape (r). In pea plants that are heterozygous for seed shape, the round seed shape is dominant over the wrinkled seed shape and the genotype is (Rr).


    Biology (A)

    In all of Mendel’s experiments, he worked with traits where a single gene controlled the trait and where one allele was always dominant to the other. Although the rules that Mendel derived from his experiments explain many inheritance patterns, the rules do not explain them all. There are in fact exceptions to Mendel’s rules, and these exceptions usually have something to do with the dominant allele.

    One exception to Mendel’s rules is that one allele is always completely dominant over a recessive allele. Sometimes an individual has an intermediate phenotype between the two parents, as there is no dominant allele. This pattern of inheritance is called incomplete dominance.

    An example of incomplete dominance is the color of snapdragon flowers. One of the genes for flower color in snapdragons has two alleles, one for red flowers and one for white flowers. A plant that is homozygous for the red allele will have red flowers, while a plant that is homozygous for the white allele will have white flowers. On the other hand, the heterozygote will have pink flowers (Figure below ). Neither the red nor the white allele is dominant, so the phenotype of the offspring is a blend of the two parents.

    Pink snapdragons are an example of incomplete dominance.

    Another example of incomplete dominance is sickle cell anemia, a disease in which the hemoglobin protein is produced incorrectly and the red blood cells have a sickle shape. A person that is homozygous recessive for the sickle cell trait will have red blood cells that all have the incorrect hemoglobin. A person who is homozygous dominant will have normal red blood cells. And because this trait has an incomplete dominance pattern of expression, a person who is heterozygous for the sickle cell trait will have some misshapen cells and some normal cells (Figures below and below ). These heterozygous individuals have a fitness advantage they are resistant to severe malaria. Both the dominant and recessive alleles are expressed, so the result is a phenotype that is a combination of the recessive and dominant traits.

    Sickle cell anemia causes red blood cells to become misshapen and curved (upper figure) unlike normal, rounded red blood cells (lower figure).

    Sickle cell anemia causes red blood cells to become misshapen and curved (upper figure) unlike normal, rounded red blood cells (lower figure).

    An example of a codominant trait is ABO blood types (Figure below ), named for the carbohydrate attachment on the outside of the blood cell. In this case, two alleles are dominant and completely expressed (designated I A and I B ), while one allele is recessive (i). The I A allele encodes for red blood cells with the A antigen, while the I B allele encodes for red blood cells with the B antigen. The recessive allele (i) doesn’t encode for any antigens. An antigen is a substance that provokes an immune response, your body’s defenses against disease, which will be discussed further in the Diseases and the Body's Defenses chapter. Therefore a person with two recessive alleles (ii) has type O blood. As no dominant (I A and I B ) allele is present, the person cannot have type A or type B blood.

    There are two possible genotypes for type A blood, homozygous (I A I A ) and heterozygous (I A i), and two possible genotypes for type B blood (I B i and I B I B ). If a person is heterozygous for both the I A and I B alleles, they will express both and have type AB blood with both antigens on each red blood cell. This pattern of inheritance is significantly different than Mendel’s rules for inheritance because both alleles are expressed completely and one does not mask the other.


    How Incomplete dominance can be explained at molecular level? - Biology

    It was clear that the hemoglobin molecules of persons with sickle cell anemia migrated at a different rate, and thus ended up at a different place on the gel, from the hemoglobin of normal persons (diagram, parts a and b). What was even more interesting was the observation that individuals sickle cell trait had about half normal and half sickle cell hemoglobin, each type making up 50% of the contents of any red blood cell (diagram part c). To confirm this latter conclusion, the electrophoretic profile of people with sickle cell trait could be duplicated simply by mixing sickle cell and normal hemoglobin together and running them independently on an electrophoretic gel (diagram part d). These results fit perfectly with an interpretation of the disease as inherited in a simple Mendelian fashion showing incomplete dominance. Here, then, was the first verified case of a genetic disease that could be localized to a defect in the structure of a specific protein molecule . Sickle cell anemia thus became the first in a long line of what have come to be called molecular diseases . Thousands of such diseases (most of them quite rare), including over 150 mutants of hemoglobin alone, are now known.

    B. Sickle Cell and Normal Hemoglobin

    But what was the actual defect in the sickle cell hemoglobin? Although we will investigate this question in more detail in a later case study (Web Page on Protein Structure), for now it will be helpful at least to outline the background of the discovery of just what it was that made sickle cell hemoglobin different from normal hemoglobin. It is the story of one of the first identifications of the molecular basis of a disease.

    Again, Linus Pauling at Caltech, one of the most productive and imaginative of twentieth-century biological chemists (with co-workers Harvey Itano, a graduate of St. Louis University Medical School, I.C. Wells and S.J. Singer) turned his attention to determining the actual difference between normal and sickle cell hemoglobin molecules. Breaking the protein molecules down into shorter fragments called peptides , Pauling and co-workers subjected these fragments to another separatory technique called paper chromatography .

    When this procedure is applied to samples of normal and mutant (sickle) hemoglobin molecules (alpha and beta chains) that had been broken down into specific peptides, all the spots are the same -- except for one crucial spot (shown darkened in the final chromatogram below), which represents the difference between sickle cell and normal hemoglobin.

    Two-dimensional paper chromatography of normal (Hemoglobin A) and mutant (sickle cell, Hemoglobin S) hemonglobins. The encircled in red spot represents the position of the peptide. Stryer, Biochemistry , 1995

    The fact that the spots migrate to different places on the chromatogram indicates their molecular structures must be somewhat different. Pauling and his colleagues were convinced that the difference might be no more than one or two amino acids, but it was left to biochemist Vernon Ingram at the Medical Research Council in London to demonstrate this directly. Taking the one aberrant peptide and analyzing it one amino acid at a time, Ingram showed that sickle cell hemoglobin differed from normal hemoglobin by a single amino acid, the number 6 position in the beta chain of hemoglobin. That one small molecular difference made the enormous difference in people's lives between good health and disease.

    C. Discovering the Difference Between Normal and Sickle-Cell Hemoglobin

    Royer Jr., W.E. "High-resolution crystallographic analysis of co-operative dimeric hemoglobin," J. Mol. Biol., 235, 657. Oxyhemoglobin PDB coordinates, Brookhaven Protein Data Bank.

    In overall structure, as we have already learned, a complete hemoglobin molecule consists of four separate polypeptide chains (i.e., each a long string, or polymer, of amino acids joined together end-to-end) of two types, designated the alpha and beta chains. The two a chains are alike (meaning they have the exact same sequence of amino acids), while the two beta chains are also alike.

    To familiarize yourself with the structure of the intact hemoglobin molecule, click here. (The Chime plugin is needed to view this molecule interactively.)

    You can rotate the molecule around, by clicking on it and hold the mouse button .

    • Hold down mouse button, choose-Select-Residue-HEM
    • Hold down mouse button, choose-Display-Spacefill-Van der Waals Radii
    • Hold down mouse button, choose-Select-Change color to Red

    Make sure you can distinguish the four subunits (the two a and the two b chains). Note the relative positions of the a and the b chains to each other. Hemoglobin is called a tetramer because the molecule as a whole is made up of four subunits, or parts. Find the porphyrin-based heme group and note how it is "sheltered" in a kind of groove within each polypeptide chain.

    • Hold down mouse button, choose-Select-Residue-HEM
    • Hold down mouse button, choose-Display-Spacefill-Van der Waals Radii
    • Hold down mouse button, choose-Select-Protein-Protein
    • Hold down mouse button, choose-Select-Hide-Hide Selected

    You can also switch from one to the other of several conventional modes of representing molecular structure: the space filling, ball and stick, wire, and ribbon forms, by holding down the mouse button and choosing-Display. As you will learn later, each gives you a different kind of information about the molecule's overall shape and some of its specific structural features.

    In sickle cell hemoglobin the two alpha chains are normal the effect of the mutation resides only in the # 6 position in the two beta chains (the mutant beta chains are referred to as "S" chains, as explained in the Terminology Box below). As mentioned above, each a and b polypeptide is folded around and shelters a special ring structure, the heme group , consisting of a porphyrin ring at whose center is an iron atom bound by four coordinate covalent bonds to four nitrogens of the porphyrin. It is this iron to which the oxygen binds (. The whole porphyrin structure is called the prosthetic group , a general term in protein chemistry to refer to non-polypeptide portions of the molecule that are usually the functionally active sites.

    • Hold down mouse button, choose-Display-Ball and Stick
    • Remove the HOH, Hold down mouse button, choose-Select-Residue-HOH
    • Hold down mouse button, choose-Select-Hide-Hide Selected

    Sickle hemoglobin tutorial by Eric Martz of the University of Massachusetts

    The chart below summarizes some of the terminology we have encountered in discussing the various kinds of hemoglobins and their clinical manifestations. Study this chart and learn the specific meanings of these terms. They will help you keep clear exactly what aspect of sickle cell anemia, or what component of the genetic or molecular system is being discussed.

    Normal hemoglobin (refers to the whole molecule)

    Sickle cell hemoglobin (homozygous mutant)

    Gene for normal hemoglobin alpha chain

    Gene for normal hemoglobin beta chain

    Gene for mutant hemoglobin beta chain, the sickle cell hemoglobin

    Structure of Normal Hemoglobin Molecule (HbA):

    2 alpha and 2 beta chains

    Structure of Sickle Cell Disease Molecule:

    Composition of Hemoglobin in Persons with Sickle Cell Disease

    All hemoglobin molecules consist of 2 alpha and 2 s chains

    Composition of Hemoglobin in Persons with Sickle Cell Trait:

    Half their hemoglobin molecules consist of 2 alpha and 2 beta chains, and half consist of 2 alpha and 2 s chains

    The difference in the one amino acid in the b chains of sickle cell hemoglobin must affect the way the molecules interact with one another. Pauling made a remarkable prediction about this difference in 1949, when he wrote: "Let us propose that there is a surface region on the . . . sickle cell anemia hemoglobin molecule which is absent in the normal molecule and which has a configuration complementary to a different region of the surface of the hemoglobin molecule. . . .Under the appropriate conditions [as in low oxygen or air pressure], then, the sickle cell anemia hemoglobin molecules might be capable of interacting with one another at these sites sufficiently to cause at least a partial alignment of the molecules within the cell, resulting in the erythrocyte's . . . membrane's being distorted to accomodate the now relatively rigid structures within its confines."

    Many years later is was shown that the amino acid that is substituted in the # 6 position in the beta chain forms a protrusion that quite accidentally fits into a complementary site on the beta chain of other hemoglobin molecules in the cell, thus allowing the molecules to hook together likes pieces of the play blocks called legos. The result is, as Pauling predicted, that instead of remaining in solution sickle cell hemoglobin molecules will lock together (aggregate) and become rigid, precipitating out of solution and causing the RBC to collapse. Early electron micrographs taken at the time showed dramatically that in sickle-cell hemoglobin, the molecules line up into long fibers inside the cell (see Fig. 4) forming trapezoidal-shaped crystals that have much the same shape as a sickled cell. Why this happens when oxygen tension is low and the hemoglobin becomes deoxygenated, will be discussed later.

    Electron micrograph of a negative stained fiber of deoxyhemoglobin S [From G. Rykes, R.H. Crepeau, and S.J. Edelstein. Nature 272(1978):509.]

    Electron micrograph of a sickled cell sectioned in a plane perpendicular to the long axis of the cell, showing close packing of hexagonal units, each measuring approximately 150 A between opposite sides (Stetson, J. Exp. med. 123:341-346, 1966.)

    It is interesting to note that in vitro (using solutions of hemoglobin extracted from red blood cells) studies of deoxygenation and reoxygenation of sickle-cell hemoglobin indicate the process is reversible, that is, as oxygen concentration is lowered hemoglobin molecules polymerize and form crystals, but as oxygen concentration is increased again the hemoglobin molecules can depolymerize and return to their soluble state. This can be written as:

    However when similar in vivo experimental tests are run on sickle-cell hemoglobin in whole red blood cells, the process was only reversible up to a certain duration of exposure time. After several hours, the process could no longer be reversed. The reasons for this relate back to our earlier question of what was the exact effect of the mutation on the red blood cell and its contents. When a long-term sickled cell is broken open and a "ghost" prepared, even with the hemoglobin extracted, the cell retains its sickled shape.

    In-Text Question 5 : What might you hypothesize to be the cause of this phenomenon and how would it relate to the earlier conclusion that hemoglobin, not other cell components, are the site of the mutation's effect?

    The notion that sickle cell anemia results from a specific amino acid substitution in a polypeptide was given further support by discovery, around the same time, of other hemoglobin variants with distinct molecular and physiological properties. In the mid 1940s it was found that Hemoglobin F, or fetal hemoglobin, has an electrophoretic mobility and a different affinity (higher) for oxygen than adult hemoglobin (fetal hemoglobin is produced by the fetus during gestation, and is slowly replaced by synthesis of the adult form in the first few months of life the higher affinity of fetal hemoglobin for oxygen facilitates the transfer of oxygen across the placenta from the mother's blood to that of the fetus). Hemoglobin F was also found to have a different amino acid sequence, indeed producing a distinctive chain, the g (gamma) chain instead of the b chain, during most of fetal life (for more details see Stryer, p. 154). Then, in the early 1950s two other hemoglobin-based conditions, designated Hemoglobin C and Hemoglobin D, were discovered by Harvey Itano in two separate families. These hemoglobins were also found to have different eletrophoretic mobilities and different amino acid sequences, as well as unique physiological effects (not as severe, however, as sickle cell hemoglobin).

    To learn more about other hemoglobinopathies, click on the following website http://sickle.bwh.harvard.edu/hemoglobinopathy.html

    Taken together, these examples all supported the general paradigm that mutations produced alterations in the amino acid sequence of proteins that, in turn, had significant effects on the protein's function. Such a conception, coming as it did at just about the time of the development of the Watson-Crick model of DNA in 1953, helped launch the revolution in molecular biology that we are still experiencing today.

    We will also explore in a later case study how at the DNA level the genetic mutation for sickle cell hemoglobin alters the specific structure of the beta polypeptide chain.


    Summary: What Is the Difference Between Incomplete Dominance and Codominance?

    Incomplete dominance and codominance are two types of genetic inheritance, and while both are variants on the standard dominant/recessive traits, it’s important to know the difference between incomplete dominance and codominance.

    Incomplete dominance is when the phenotypes of the two parents blend together to create a new phenotype for their offspring. An example is a white flower and a red flower producing pink flowers. Codominance is when the two parent phenotypes are expressed together in the offspring. An example is a white flower and a red flower producing offspring with red and white patches.

    Being able to explain the difference between incomplete dominance and codominance will help you understand different inheritance patterns and be able to answer genetics questions (especially = incomplete dominance vs. codominance questions) much more easily.


    Incomplete Dominance And Codominance

    An excellent example of the blending of phenotypes is the species of snapdragon called Antirrhinum majus, which will produce pink flowers if homozygous white flowers and homozygous red flowers combine their DNA. This is an example of incomplete dominance. Another example of incomplete dominance in the Andalusian chicken, which is native to Spain and exhibits incomplete dominance in the coloration of its feathers. If a black female Andalusian chicken and a white male chicken breed they will frequently produce offspring who have feathers with blue tinges. This reflects how the mixed alleles dilute the pigment melanin and cause the feathers to be lighter in coloration.

    Beyond incomplete dominance, a phenotypic phenomenon called co-dominance can occur. In this case, both alleles are simultaneously expressed win the heterozygotic organism. There are actually groups of people who have a blood type known as MN, and what determines this blood type is the alleles of certain genes. A person with an L^m allele shows an M marker on the surface of their red blood cells, while people with L^n markers show a different N red blood cell marker. While homozygous people only have one of the two markers on their red blood cells, heterozygous people display two of them, a perfect example of co-dominance where both phenotypes are displayed.


    What is Codominance

    Codominance is a concept in which heterozygous offspring produces both alleles simultaneously without any mixing of the two parental alleles. In codominance, both parental alleles are dominantly expressed in the offspring. Both parental alleles can be observed in the offspring without blending. Thus, codominance is a qualitative approach of gene expression. Codominance mostly occurs when more than two alleles are present for the determination of the phenotype of a particular trait. Those alleles are called multiple alleles.

    Figure 1: Hybrid Red and White Camellia

    The roan cow containing both red and white hairs is an example of codominance. The AB blood group also shows codominance in humans. A cross between the red homozygous Camellia flowers and white homozygous Camellia flowers produces an offspring with both red and white spots within the same flower is shown in figure 1.


    Codominance - Incomplete Dominance

    Patrick has been teaching AP Biology for 14 years and is the winner of multiple teaching awards.

    In both codominance and incomplete dominance, both alleles for a trait are dominant. In codominance a heterozygous individual expresses both simultaneously without any blending. An example of codominance is the roan cow which has both red hairs and white hairs. In incomplete dominance a heterozygous individual blends the two traits. An example of incomplete dominance is the pink snapdragon, which receives a red allele and white allele.

    While most students get the idea between a dominance and recessive alleles what often throws them for a curve is the difference between codominance and Incomplete Dominance, so let's take a closer look at those, so these are exceptions to the whole idea about complete dominance where one allele will completely overwhelm or not allow the other alleles effects to be shown.

    In this case rather than the heterozygotes individuals looking like the homozygotes dominance, here the heterozygote, a hybrid between two types of beings, does not look anything like the true bred ones the homozygotes so what's the difference between codominance and incomplete dominance? It's how they do this effect.

    With codominance you'll see both alleles showing their effects but not blending whereas with incomplete dominance you see both alleles effects but they've been blended. Now their distinction is sometimes is hard to figure out so let me give a couple of concrete examples, so the standard example of codominance is what's known as a Roan cow. There are kind of cows that are white, there are kind of cows that are red. Now a red cow has big R big R for the hair color allele, the white cow has big W big W for the hair color allele now you may be thinking hey! I only use the capitals for the dominant why are why I'm I using two different capitals and two different letters you're supposed to use all the same letter and that's because both of these are dominant alleles so what will happen is if you have an offspring between in red and a white cow you'll get a colored cow called Roan. What happens is that you'll see white hairs and red hairs so you're seeing the effects of the white cow's hair allele and the red cow's hair allele. But you're not seeing pink hairs that would be blending and that's what incomplete dominance looks like.

    The standard example of incomplete dominance is a kind of flower called a snapdragon. With snapdragons you can have red, white or pink flowers and it turns out the pink ones are blends between the red and the white alleles so if you have big R big R you'll be a red flower. If you're big W big W you'll be a white flower, if you're big R and W you'll be pink not little bits of red and little bits of white if you're getting closer and look at the flower close it's pink it's pink it's pink they blend it, so that's the big difference between codominance, they show both effects no blending incomplete dominance it's all blended.


    Supporting information

    S1 Fig. A half-diallel population and distributions of phenotypes.

    (a) Twelve maize inbred lines were selected and crossed in a half-diallel fashion. Each inbred lines was used as both male and female and the resulting F1 seed was bulked. (b) Density plots of normalized BLUE values for the seven phenotypic traits. We used the “scale” function in R to normalize the BLUE values by first centering on zero and then dividing the numbers by their standard deviation. The seven phenotypic traits are plant height (PHT), height of primary ear (EHT), days to 50% pollen shed (DTP), days to 50% silking (DTS), anthesis-silking interval (ASI), grain yield adjusted to 15.5% moisture (GY), and test weight (TW).

    S2 Fig. Pairwise correlation plots of seven phenotypic traits.

    The upper right panels show the scatter plots of all possible pairwise comparisons of two traits. The red line is a fitted loess curve. In the lower left panels, the numbers are the Spearman correlation coefficients (r) and the asterisks (*) indicate the correlation coefficients are statistically significant (Spearman correlation test P value < 0.05). Units for various traits are plant height (PHT, in cm), height of primary ear (EHT, in cm), days to 50% pollen shed (DTP), days to 50% silking (DTS), anthesis-silking interval (ASI, in days), grain yield adjusted to 15.5% moisture (GY, in bu/A), and test weight (TW, weight of 1 bushel of grain in pounds).

    S3 Fig. Haplotype block identification using an IBD approach.

    In the upper panel, regions in red are IBD blocks identified by pairwise comparison of the two parental lines of a hybrid. The vertical dashed lines define haplotype blocks. In the lower panel, hybrid genotypes in each block are coded as heterozygotes (0) or homozygotes (1).

    S4 Fig. The minor allele frequency estimated from 12 parental lines in bins of 0.01 GERP score.

    Red solid and grey dashed lines define the best-fit regression line and its 95% confidence interval.

    S5 Fig. Segregating genetic load across ten maize chromosomes.

    ots indicate mean GERP scores of putatively deleterious SNPs (GERP scores > 0) carried by the 12 parental maize lines (bin size = 1 cM). Vertical red lines indicate centromeres.

    S6 Fig. Cumulative variance explained by GERP-SNPs.

    Additive and dominance effects are indicated by red and blue colors respectively.

    S7 Fig. Phenotypic variance explained for observed data and for randomly shuffled data using the genomic selection model.

    Histograms show the results for the randomly shuffled (10 times) degrees of dominance (k) in each trait. Red lines show the phenotypic variance explained using the observed k.

    S8 Fig. Linear regressions of GERP-SNPs’ additive variance, dominance variance and total variance of seven traits per se against their GERP scores.

    Solid and dashed lines represent significant and non-significant linear regressions, with grey bands representing 95% confidence intervals. Data are only shown for SNPs which explain more phenotypic variance than the genome-wide mean.

    S9 Fig. Linear regressions after filtering out GERP-SNPs located in regions in the lowest quartiles of recombination.

    Solid and dashed lines represent significant and non-significant linear regressions, with grey bands representing 95% confidence intervals. Data are only shown for GERP-SNPs which explain more variance than the genome-wide mean and found in regions above the first quantile of the recombination rate (cM/Mb).

    S10 Fig. Phenotypic variance explained for grain yield and degree of dominance (k) of GERP-SNPs after removing 11 hybrids that B73 as one parent.

    (a) Total per-SNP variance explained for grain yield per se by deleterious (red lines) and randomly sampled SNPs (grey beanplots). (b) Density plots of the degree of dominance (k). Extreme values of k were truncated at 2 and -2 for visualization. (c-e) Linear regressions of additive effects (c), dominance effects (d), and degree of dominance (e) of seven traits per se against SNP GERP scores. Colors in (c-e) are the same as the legend for (b). Solid and dashed lines represent significant and nonsignificant linear regressions, with grey bands representing 95% confidence intervals. Data are only shown for deleterious alleles that explain more variance than the genome-wide mean.

    S11 Fig. Regression of degree of dominance (k) on GERP scores for simulated data.

    The solid blue line indicates the regression line fitted to data simulated under mutation-selection balance (see Methods for details).

    S12 Fig. Cross-validation accuracy using GERP-SNPs in genic regions.

    Beanplots represent prediction accuracy estimated from cross-validation experiments for traits per se (a, b, c) and heterosis (d, e, f) under additive (a, d), dominance (b, e), and incomplete dominance (c, f) models. Prediction accuracy using real data is shown on the left (green) and permutation results on the right (grey). Horizontal bars indicate mean accuracy and the grey dashed lines indicate the overall mean accuracy. Stars indicate real data having significantly (t-test P value < 0.05) higher cross-validation accuracy than permuted data.

    S13 Fig. Cross-validation prediction accuracy for trait per se and heterosis.

    Beanplots represent prediction accuracy estimated from cross-validation experiments for traits per se (a, b) and heterosis (c, d) under additive (a, c) and dominance (b, d) models. Prediction accuracy using real data is shown on the left (red) and permutation results on the right (grey). Horizontal bars indicate mean accuracy of each trait and the grey dashed lines indicate the mean accuracy of all traits. Stars indicate real data having significantly (t-test P value < 0.05) higher cross-validation accuracy than permuted data.

    S14 Fig. Breeding values of grain yield for diploid and simulated triploid hybrids.

    Each line represents the posterior breeding values of a diploid hybrid (red circle), its best parent (black diamond), and predicted breeding values of simulated AAB triploid (blue square) and ABB triploid (green triangle) plants based on estimated effect sizes and dominance values for each SNP.

    S1 Table. Best Linear Unbiased Estimator (BLUE) values and levels of heterosis of the seven phenotypic traits for the 66 hybrids.

    Abbreviations for phenotypic traits are plant height (PHT, in cm), height of primary ear (EHT, in cm), days to 50% pollen shed (DTP), days to 50% silking (DTS), anthesis-silking interval (ASI, in days), grain yield adjusted to 15.5% moisture (GY, in bu/A), and test weight (TW, weight of 1 bushel of grain in pounds).



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