Most of these are specific to men and are found on the X chromosome. Remember, men have an X and a Y chromosome while women have two X's. What this means is that men have a single copy of each gene on the X and the Y. So if a male is not colorblind, we know his genotype even though colorblindness is dominant. This is because the gene is on the X chromosome and the man has just a single copy of the gene. He has a single copy of the dominant version of the gene that lets him distinguish red from green.
So we know his genotype. And there are other X- and Y-linked traits like this too. Bottom line is you can't always figure out genotype from phenotype with a dominant trait because dominant traits can happen with two different genotypes. But there are a few special situations where you can tell the genotypes apart. By Dr. Barry Starr, Stanford University. Why some gene copies are recessive Lots of traits you learned about in school are not really dominant Figuring out if a trait is dominant or recessive.
Brown eyes can be caused by two genotypes. If a parent has a recessive trait, all the kids will have at least one recessive gene copy. The Tech Interactive S. Market St. San Jose, CA The Tech is a registered c 3. Federal ID Its content is solely the responsibility of the authors and does not necessarily represent the official views of Stanford University or the Department of Genetics. The Tech Interactive. Stanford The Tech Ask a Geneticist Commonly Asked Questions Categories I find this all very confusing but if a person has a dominant trait, can they know their genotype for certain?
Dominant vs. Back to Dominant vs. Let's say you can taste it. What is your genotype? If it tastes bitter, you have the dominant trait.
Genetic Testing and Family Trees An obvious way to figure out you genotype is to have a genetic test done. Imagine that your mom can't taste PTC. Now we know your genotype! Other Ways to Figure Out Genotype In some cases you can make a pretty good guess at your genotype even without a genetic test or the right family history.
If a trait is on the X or Y and you are male, then we know your genotype. More Information Why some gene copies are recessive Lots of traits you learned about in school are not really dominant Figuring out if a trait is dominant or recessive. A major conceptual advance made by Charles Darwin was to relate variation among individuals within an interbreeding group difference 2 with variation between taxonomic groups in space and time difference 1; Lewontin, a.
Importantly, the GP difference is always defined relative to a population, or taxon, of interest Sober, In less medically developed countries, humans carrying two defective copies of the phenylalanine hydroxylase gene have serious medical problems including seizure and intellectual disabilities.
In contrast, in most developed countries, such humans are diagnosed at birth and have a normal life span with normal mental development thanks to a phenylalanine-restricted diet Armstrong and Tyler, Therefore the GP relationship involving the phenylalanine hydroxylase defective mutation is context-dependent: the mutation is associated with health problems in less medically developed countries but not in other countries.
In summary, the GP relationship is best viewed as a relationship between two variations, one at the genotypic level, and one at the phenotypic level. The human mind can elaborate concepts of increasing abstraction: concepts of things e.
Here the concept of GP relationship establishes a relation between two changes genetic and phenotypic. In the next paragraphs we will show that, compared to the usage of intuitive concepts of things, this detour through increased abstraction may prove more efficient to better understand phenotypic diversity. We argued above that the differential view should always be kept in mind when thinking about the connection between genotypes and phenotypes.
GWAS, which represent the most popular method to detect genomic loci that are associated with complex traits in populations, are based on the analysis of differences Visscher et al.
Nevertheless, in current research the differential view is sometimes implicitly dismissed. When multiple factors are observed to influence phenotypic traits Figure 1B , the differential view is considered as too simplistic and researchers often prefer to focus back on phenotypes of single individuals, without explicitly relating them to a phenotypic reference.
In most current articles, the problem of connecting the genotype to the phenotype is framed in terms of genotype and phenotype maps. He indicated the average genotype of a population as a point in the space of all possible genotypes G space and the average phenotype of the same population as a corresponding point in the space of all possible phenotypes P space.
The evolutionary process was thus decomposed into four steps: 1 the average phenotype is derived from the development of the distinct genotypes in various environments; 2 migration, mating, and natural selection acts in P space to change the average phenotype of the initial population into the average phenotype of the individuals which will have progeny; 3 the identity of successful parents determines which genotypes are preserved; and 4 genetic processes such as mutation and recombination modify position in G space.
Three current graphical representations of GP maps. A The early version of the GP map proposed by Lewontin a. B A GP map where each point represents a single individual Houle et al. C The relationships between traits and genes, as depicted by Wagner See text for details. In another common graphical representation Figure 2B , a point in the G space and its corresponding point in the P space correspond to the genotype and the phenotype of a single individual Fontana, ; Landry and Rifkin, In a third representation put forward by Wagner ; Figure 2C , individual genes are connected to individual traits.
Although these three graphical representations of GP maps may facilitate our understanding of certain aspects of biology, in all of them the GP relationship and the differential view are not easy to grasp. It is quite perplexing that the first person to draw such a GP map was Richard Lewontin, an eloquent advocate of the differential view see for example his preface to Oyama, , a masterpiece of persuasion.
Because these graphics focus on individual rather than differential objects, we believe that these three representations implicitly incite us to go back to the more intuitive idea of one genotype associated with one phenotype. Losing sight of the differential view might also come from the molecular biology perspective, where proteins are viewed as having causal effects on their own, such as phosphorylation of a substrate or binding to a DNA sequence.
Because of the two entangled definitions of the gene, either as encoding a protein, or as causing a phenotypic change Griffiths and Stotz, , it is easy to move from a differential view to a non-differential view of the GP relationship.
In summary, many current mental representations of the connection between genotype and phenotype implicitly dismiss the differential view. We will now show that the differential view is compatible with the fact that phenotypic traits are influenced by a complex combination of multiple factors and that we can find a relevant schematic representation of GP relationships.
Decomposing an organism into elementary units such as anatomical structures has been instrumental in many biology disciplines such as physiology, paleontology and evolution. However, the issue is to identify the decomposition into characters that is most adequate for the question of interest. For questions related to relationships between organs of various individuals or species such as homology , it might be appropriate to keep the traditional decomposition into anatomical structures Wagner, Their definition deals with absolute traits observed in single organisms for example the shape of a wing, or the number of digits in an individual and is thus far from the differential view.
Here, to better apprehend evolution and phenotypic diversity of the living world, we propose to decompose the observable attributes of an organism into multiple elementary GP variations that have accumulated through multiple generations, starting from an initial state. We insist that under this perspective, characters are not concrete objects such as skin but abstract entities defined by the existence of differences between two possible observable states for example skin color. As an analogy, one can imagine two ways to produce a well-worn leather shoe of a particular shape.
One can either assemble the different atoms into the same organization, or one can buy a shoe in a store and then subject it to a series of mechanical forces. We are naturally inclined to compare organisms to machines, and to think in terms of pieces that must be assembled to make a functional whole. However, the rampant metaphor of the designer or maker is inadequate for understanding the origin of present-day organisms Coen, To understand the phenotypic features of a given organism it is more efficient to decompose it into abstract changes that occurred successively across evolutionary time, and not across developmental time.
The initial state is a hypothetical ancestor of the organism under study. Certain mutations qualified as pleiotropic are observed to affect several organs at once while others alter only one at a time Paaby and Rockman, ; Zhang and Wagner, For pleiotropic mutations, we consider that the GP relationship should include all the phenotypic changes in diverse organs, at various stages, etc.
For instance, the VA mutation of the EDAR receptor is associated not only to hair thickness but also to changes in sweat gland and mammary gland density in Asian populations Kamberov et al. The GP relationship is, in such cases, one-to-multi. Considering skin and eye as independent anatomical modules of the human body might seem appropriate for many evolutionary changes, but it is somewhat inadequate in cases where these two organs evolved a new pigmentation trait at once through a single mutation in the SLC45A2 gene Liu et al.
Reasoning in terms of GP relationships strikes off the problem of finding a relevant decomposition into elementary anatomical structures. The elementary GP relationships themselves appear as adequate semi-independent modules, whose combination can account for the observable characteristics of an organism. Under the differential concept of GP relationships, one crucial point is to decompose observable traits into a series of semi-independent phenotypic variations, that is to identify the elementary changes that have occurred during evolution.
Experimental approaches are available to decompose a given phenotypic difference into appropriate finer sub-variations. For example, crossing plants with different leaf shapes yields a progeny that exhibits a composite range of intermediate leaf shapes.
Principal component analysis uncovered elementary leaf shape changes that can together account for the difference in shape between parental lines and that appear to be caused by distinct genomic regions Langlade et al. Another illuminating example is the abdominal pigmentation in the Drosophila dunni group.
Taken as a single variable, the levels of pigmentation show a complex genetic architecture, but decomposing adult patterns into anatomical sub-units unravels discrete genetic control for each sub-trait Hollocher et al. A better known case is the evolution of body color in beach mice. The difference in color between light-colored beach mice and dark mice can be decomposed into distinct phenotypes dorsal hue, dorsal brightness, width of tail stripe, and dorsoventral boundary , which are all associated with distinct mutations in the Agouti gene Linnen et al.
Each Agouti genetic locus appears to be dedicated to the specification of pigmentation in a given body part. Together, they form a group of tightly linked loci that are associated with changes in coat pigmentation. Evolution of light-colored beach mice is caused by several mutations with distinct pigmentation effects in the Agouti locus. The dark and light phenotypes can be decomposed into four phenotypic traits, which are associated with different single nucleotide polymorphisms SNPs, colored dots located in the Agouti gene.
Only SNPs with inferred selection coefficient of the light allele higher than 0. Coding exons are represented as dark boxes and untranslated exons as white boxes. Adapted from Linnen et al. While complex traits may not always be reducible to a suite of simple GP relationships, it is possible that traits such as adult human height, the most emblematic quantitative trait predicted to consist of many genetic effects of small size Fisher, , might also be decomposed into elementary variations, each explaining more discrete sub-traits.
While some determinants of human height such as LIN28B have been associated to adult height at different ages, other genes have only reached statistical significance in stage-specific studies focusing on fetal growth and height velocity at puberty Lettre, In other words, these data suggest that human height may be a composite trait that is modulated by several GP relationships, each acting at different phases of developmental growth.
Gene-by-Environment GxE interaction occurs when the phenotypic effect of a given genetic change depends on environmental parameters. Similarly, epistasis, or GxG interaction, occurs when the phenotypic effect of a given genetic change depends on the allelic state of at least one other locus Phillips, ; Hansen, There is increasing evidence that GxG and GxE interactions are of fundamental importance to understand evolution and inheritance of complex traits Gilbert and Epel, ; Hansen, We propose that both phenomena can be integrated into the basic GP differential framework, where both GxG and GxE interactions inject a layer of context-dependence, and result in differences embedded within differences.
The difference in color pigmentation between dark and light-colored beach mice mentioned previously Figure 3 is not only due to mutations in Agouti but also to a coding mutation in the MC1R gene that decreases pigmentation Steiner et al. The effect of the MC1R mutation is visible only in presence of the light-colored-associated derived Agouti haplotype.
Here the Mc1R locus is considered to interact epistatically with the Agouti locus. In this case, we propose that the GP relationship does not comprise a single phenotypic difference but two possible phenotypic differences a change in coat pigmentation or no change at all. The choice between these two phenotypic differences is determined by the genetic background here at the Agouti locus.
The differential view thus remains relatively straightforward for two-loci interactions: the context-dependence of the phenotype is translated into a choice between two possible phenotypic differences. We propose that a GP relationship involving a mutation subjected to multiple epistatic interactions should comprise all possible phenotypic differences that can result from the mutation in all genetic backgrounds.
Among all possible phenotypic variations, the phenotypic difference that will be observed is determined by other genetic loci. In general, GxG interactions involve multiple sites that are dispersed across the genome Bloom et al. Gene-by-environment GxE and GxG interactions. B The Mc1R coding mutation affects mouse body pigmentation in presence of dominant light alleles of Agouti but not in an Agouti homozygous background for the recessive dark allele Steiner et al.
An example of GxE interaction see also Figure 4A is the naturally occurring loss-of-function allele of brx in Arabidopsis plants, which is associated with accelerated growth and increased fitness in acidic soils, and with severely reduced root growth compared to wild-type in normal soils Gujas et al. GxE interactions are usually analyzed in the form of a norm of reaction , which represents all the observable traits of a single genotype across a range of environments Johannsen, ; Sarkar, In the case of GxE interactions, we propose that the GP relationship should comprise all the possible phenotypic changes that can be caused by the associated genetic change across various experimental conditions.
The associated phenotypic change is thus a difference between two norms of reaction. A textbook example is the variation in temperature-size rule in C. Like most other animals, C. An amino acid change in a calcium-binding protein is responsible for the decreased ability of the Hawaiian strain to grow larger at low temperature Kammenga et al. Here the norm of reaction representing nematode body size across a range of temperatures differs between nematodes and the associated GP relationship encompasses the difference between these two slopes.
The range of phenotypic variations embodied within GP relationships subjected to GxG and GxE interactions can be quite overwhelming, especially in cases when several tissues are affected by the same mutation, and when the phenotypic variation of each tissue is influenced by other genomic loci and by environmental conditions. In fact, the phenotypic effects of a mutation always rely on other pieces of DNA from the same genome, so that any GP relationship can be considered to experience epistasis.
In other words, a genetic locus affecting a phenotype never acts independently of other DNA sequences. For instance, a given opsin allele will only lead to particular color vision properties if an eye is formed and if this eye receives light during its development, allowing effective vision neural circuits to form. For the differential view to be tractable, we advise not to consider all possible genetic backgrounds and environmental conditions, but to restrict possibilities to potential environments, and segregating alleles that are relevant to the population of interest Sober, In summary, in presence of epistasis or GxE interactions, a genetic change is not associated with a single phenotypic difference but with multiple possible phenotypic differences, among which one will be achieved, depending on the environment and the genetic background.
The context-dependence can be represented schematically as GP differences embedded into other genotype and environment differences.
As underlined by multiple authors most notably Waddington, ; Oyama, ; Keller, , genes and environment act jointly on the phenotype, and in most cases it is impossible to disentangle the effect of one from the other. Here we show that reasoning in terms of differences helps to clarify the comparison between genetic and environmental effects on phenotypes. However, we identify certain cases where the comparison remains difficult.
By analogy with the GP relationship, we can define the environment-phenotype relationship as an environmental variation two environments , its associated phenotypic change distinct phenotypic states , and their relationships. In this case, environmental and genetic effects can be compared: sex chromosomes and temperature have the same phenotypic effect on turtles. West-Eberhard , extrapolated from differences segregating within populations difference 2 to differences that arose temporally during the evolution of a population difference 1.
Environment—phenotype relationship vs. GP relationship for sex determination in turtles. A In some species, the temperature during embryonic development determines the sex of the adult. B In others, sex is determined by sex chromosomes. For instance, the strongest claw of a lobster will develop based on usage and has a priori equal probabilities to develop on the left or on the right side.
This example shows that for the sake of accuracy it is important to explicitly state the differences that are being considered within a GP relationship. The differential view provides a theoretical framework that can help in designing experiments to investigate the proper variables: one can compare different genotypes in a fixed environment classic GP relationship , compare the response of a fixed genotype to two different environments phenotypic plasticity , or compare the sensitivity of two different genotypes to two different environments wherein the phenotypic variation becomes a difference in a difference ; see for example Engelman et al.
Various quantitative methods have been developed to disentangle genetic from environmental effects and to quantify GxE interactions Lynch and Walsh, Yet in certain situations it can be impossible to separate genetic from environmental effects in a biologically meaningful way, even when reasoning in terms of differences Lewontin, b.
Populations of the beetle Calathus melanocephalus comprise two morphs, long-winged, and short-winged Schwander and Leimar, The long-winged morph only develop from homozygous individuals for a recessive allele segregating in the population, and only when food conditions are good. In this case, the genetic and environmental effects are intermingled Figures 6A,B.
In the theoretical case of a population comprising only short-winged heterozygous animal that have been raised in starving conditions and long-winged ones, both genes and environment are responsible for the wing difference between individuals and it is impossible to estimate the proportion of environmental and genetic effects because genes and environment act on distinct levels along the complex causal link between genotypes and phenotypes.
The environment-phenotype relationship and GP relationship perspectives for wing length polymorphism in the beetle Calathus melanocephalus. A Under the environment-phenotype relationship perspective, a change in food conditions is associated with a change in wing size, but only in a homozygous background for the recessive allele l of the wing size locus. B Under the GP relationship perspective, a genetic change at the wing size locus is associated with a change in wing size, but only in good food conditions.
Mice fed with a Lactobacillus strain of bacteria show reduced anxiety-related behaviors compared to control mice fed with broth without bacteria Bravo et al. Here the behavioral difference is caused by a switch between presence or absence of a particular gut symbiont. The cause of the phenotypic difference is not a simple change in a DNA sequence, nor a simple environmental change disconnected from genetic changes, but a switch between presence and absence of a factor that can be considered as an environmental factor — the bacteria — which contains DNA whose mutations may also change the host phenotype.
In conclusion, reasoning in terms of differences can help to clarify the comparison between genetic and environmental effects on phenotypes. However, the issues are nothing but simple. Since genes and environment act on distinct levels along the complex causal link between genotypes and phenotypes, in certain cases it is impossible to disentangle both causes.
The differential perspective makes it evident that a loss of phenotype is not necessarily associated with a loss of genetic material, and vice versa.
Furthermore, as one of us noted previously appendix of Stern and Orgogozo, , gain or loss for a phenotype is subjective. For example, loss of hair might also be considered as gain of naked epidermis.
Most insect epidermal cells differentiate into one of these two alternative states and both states involve large gene regulatory networks.
It is not clear which phenotypic state represents a gain or loss relative to the other. Even on the genotypic side, defining losses and gains can be difficult.
The insertion of a transposable element can knock down a gene, whereas a deletion can sometimes creates a new binding site for an activator of transcription. As a matter of fact, the evolutionary gain of desatF expression in D. Similarly, the differential perspective on environmental effects highlights the fallacy of the distinction between permissive and instructive signals.
As argued above, these distinctions at the phenotypic level are not clear-cut. A mutation is expected to produce a somewhat reproducible phenotypic variation within a population. Such reproducibility in phenotypic outcome is required to allow genetic evolution and adaptation by natural selection Lewontin, a ; Kirschner and Gerhart, Indeed, a newly formed allele that would generate yet another phenotype each time it ends up in a different organism would not be subjected to natural selection.
Reasoning in terms of variation, rather than considering alleles as isolated entities, makes it clear that competition occurs between alleles that span the same genetic locus. Natural selection acts directly on the allelic variation that is consistently associated with a given phenotypic variation, which is the GP relationship itself.
The GP relationship is thus a basic unit of evolutionary change, on which natural selection acts. A major discovery of the past 20 years is that variation at certain genetic loci produce comparable phenotypic variation not only in various individuals of one population, but also in extremely diverse taxa Martin and Orgogozo, b.
In other words, certain GP relationships are taxonomically robust and present across a large range of species. This implies that the genetic and environmental backgrounds have remained relatively constant or have appeared repeatedly throughout evolution to allow for genetic loci to generate similar phenotypic changes in various taxonomic groups.
This important finding was quite unsuspected some 50 years ago. For a long time the singularity observed in the living world was expected to reflect a comparable singularity at the genetic level, implicating disparate and non-conserved genes, specific to each lineage Mayr, In other words, the genetic loci that make a man a man were expected to be different from the ones that make a dog, or a fish. Later, in the 80—90s, a few researchers suggested quite the contrary that evolution proceeds through mutations in conserved protein-coding genes Romero-Herrera et al.
As of today, the accumulating data on the mutations responsible for natural variation make it clear that the diversity in living organisms share a common genetic basis on at least three points.
First, comparative developmental biology revealed that animals share common sets of key regulatory genes with conserved functions Wilkins, , ; Carroll et al. Third, multiple cases of similar phenotypic changes have been shown to involve mutations of the same homologous genes in independent lineages Table 1 , sometimes across large phylogenetic distances. For instance, the difference in pigmentation between white and orange Bengal tigers has recently been mapped to a single mutation in the transporter protein gene SLC45A2 Xu et al.
A more dramatic example is the recent evolution of a toxin resistance in three species that diverged more than million years ago — a clam, a snake and a pufferfish — via the same amino acid substitution in a conserved gene Bricelj et al. Such striking patterns of genetic repetition have now been found for more than genes in animals and plants Martin and Orgogozo, b.
Despite existing methodological biases favoring conserved genes in the search for quantitative trait loci Rockman, ; Martin and Orgogozo, b , the level of genetic repetition remains astounding and suggests that for the evolution of at least certain phenotypic differences, relatively few genetic roads lead to Rome Stern, Nowadays, one should not be surprised that a piece of DNA associated with a complex wing color pattern in one Heliconius butterfly species provides similar wings and collective protection from the same predators when introduced into the genome of other butterflies Supple et al.
What makes a dog a dog or a man a man is now partly explained by singular assortments of taxonomically robust GP relationships, which are found in multiple lineage branches. Certain environment—phenotype relationships are also taxonomically robust. For example, across most taxa body size is affected by nutrition; iron deficiency can cause anemia and certain toxic compounds can be lethal.
In ectotherms the temperature of the organism depends on the environmental temperature. The Punnett square in Figure 8 can be used to consider how the identity of the unknown allele is determined in a test cross.
Again, the Punnett squares in this example function like a genetic multiplication table, and there is a specific reason why squares such as these work. During meiosis, chromosome pairs are split apart and distributed into cells called gametes. Each gamete contains a single copy of every chromosome, and each chromosome contains one allele for every gene. Therefore, each allele for a given gene is packaged into a separate gamete. For example, a fly with the genotype Bb will produce two types of gametes: B and b.
In comparison, a fly with the genotype BB will only produce B gametes, and a fly with the genotype bb will only produce b gametes. Figure A monohybrid cross between two parents with the Bb genotype. Figure Detail The following monohybrid cross shows how this concept works.
The principle of segregation explains how individual alleles are separated among chromosomes. But is it possible to consider how two different genes, each with different allelic forms, are inherited at the same time? For example, can the alleles for the body color gene brown and black be mixed and matched in different combinations with the alleles for the eye color gene red and brown?
The simple answer to this question is yes. When chromosome pairs randomly align along the metaphase plate during meiosis I, each member of the chromosome pair contains one allele for every gene. Each gamete will receive one copy of each chromosome and one allele for every gene. When the individual chromosomes are distributed into gametes, the alleles of the different genes they carry are mixed and matched with respect to one another. In this example, there are two different alleles for the eye color gene: the E allele for red eye color, and the e allele for brown eye color.
The red E phenotype is dominant to the brown e phenotype, so heterozygous flies with the genotype Ee will have red eyes. Figure The four phenotypes that can result from combining alleles B, b, E, and e. When two flies that are heterozygous for brown body color and red eyes are crossed BbEe X BbEe , their alleles can combine to produce offspring with four different phenotypes Figure Those phenotypes are brown body with red eyes, brown body with brown eyes, black body with red eyes, and black body with brown eyes.
Consider a cross between two parents that are heterozygous for both body color and eye color BbEe x BbEe. This type of experiment is known as a dihybrid cross. All possible genotypes and associated phenotypes in this kind of cross are shown in Figure The four possible phenotypes from this cross occur in the proportions Specifically, this cross yields the following:.
Why does this ratio of phenotypes occur? To answer this question, it is necessary to consider the proportions of the individual alleles involved in the cross. The ratio of brown-bodied flies to black-bodied flies is , and the ratio of red-eyed flies to brown-eyed flies is also This means that the outcomes of body color and eye color traits appear as if they were derived from two parallel monohybrid crosses. In other words, even though alleles of two different genes were involved in this cross, these alleles behaved as if they had segregated independently.
The outcome of a dihybrid cross illustrates the third and final principle of inheritance, the principal of independent assortment , which states that the alleles for one gene segregate into gametes independently of the alleles for other genes. To restate this principle using the example above, all alleles assort in the same manner whether they code for body color alone, eye color alone, or both body color and eye color in the same cross.
Mendel's principles can be used to understand how genes and their alleles are passed down from one generation to the next. When visualized with a Punnett square, these principles can predict the potential combinations of offspring from two parents of known genotype, or infer an unknown parental genotype from tallying the resultant offspring.
An important question still remains: Do all organisms pass on their genes in this way? The answer to this question is no, but many organisms do exhibit simple inheritance patterns similar to those of fruit flies and Mendel's peas. These principles form a model against which different inheritance patterns can be compared, and this model provide researchers with a way to analyze deviations from Mendelian principles.
This page appears in the following eBook. Aa Aa Aa. Genes come in different varieties, called alleles. Somatic cells contain two alleles for every gene, with one allele provided by each parent of an organism. Often, it is impossible to determine which two alleles of a gene are present within an organism's chromosomes based solely on the outward appearance of that organism.
However, an allele that is hidden, or not expressed by an organism, can still be passed on to that organism's offspring and expressed in a later generation. Tracing a hidden gene through a family tree. Figure 1: In this family pedigree, black squares indicate the presence of a particular trait in a male, and white squares represent males without the trait. White circles are females. A trait in one generation can be inherited, but not outwardly apparent before two more generations compare black squares.
Figure Detail. The family tree in Figure 1 shows how an allele can disappear or "hide" in one generation and then reemerge in a later generation. In this family tree, the father in the first generation shows a particular trait as indicated by the black square , but none of the children in the second generation show that trait.
Nonetheless, the trait reappears in the third generation black square, lower right. How is this possible?
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