Biological Inheritance: Meaning, Categories, Specifications and Mendel’s Laws

Let us make an in-depth study of the biological inheritance. After reading this article you will learn about 1. Meaning of Biological Inheritance 2. Categories of Biological Inheritance 3. Specifications of Biological Inheritance 4. Mendel’s Laws 5. Types of Dominances and 6. Autosomal Dominant Gene.

Meaning of Biological Inheritance:

Biological inheritance is the process by which an offspring cell or organism acquires or becomes predis­posed to characteristics of its parent cell or organism. Through inheritance, variations exhibited by indi­viduals can accumulate and cause a species to evolve. The study of biological inheritance is called genetics.

Categories of Biological Inheritance:

The description of a mode of biological inherit­ance consists of three main categories:

1. Number of involved loci:

i. Monogenetic (also called ‘simple’)—one locus

ii. Oligogenetic—few loci

iii. Polygenetic—many loci

2. Involved chromosomes:

(a) Autosomal—Loci are not situated on a sex chromosome

(b) Gonosomal—Loci are situated on a sex chromosome

(c) X-chromosomal—Loci are situated on the X chromosome (the more common case)

(d) Y-chromosomal—Loci are situated on the Y chromosome

(e) Mitochondrial—Loci are situated on the mitochondrial DNA

3. Correlation genotype-phenotype:

i. Dominant

ii. Intermediate (also called ‘co-dominant’)

iii. Recessive

These three categories are part of every exact description of a mode of inheritance in the above order.

Specifications of Biological Inheritance:

Additionally, more specifications may be added as follows:

1. Coincidental and environmental interactions:

i. Penetrance

ii. Incomplete (percentual number)

iii. Invariable

iv. Complete

v. Expressivity

vi. Variable

vii. Maternal or paternal imprinting phenomena

viii. Heritability (in polygenetic and sometimes also in oligogenetic modes of inheritance)

2. Sex-linked interactions:

A. Sex-linked inheritance (gonosomal loci)

B. Sex-limited phenotype expression (ex. Cryptorchism)

C. Inheritance through the maternal line (in case of mitochondrial DNA loci)

D. Inheritance through the paternal line (in case of Y-chromosomal loci)

3. Locus-locus-interactions:

a. Epistasis with other loci (ex. Over-dominance)

b. Gene coupling with other loci

c. Homozygotes lethal factors

d. Semi-lethal factors

Determination and description of a mode of inheritance is primarily achieved through statistical analysis of pedigree data. In case the involved loci are known, methods of molecular genetics can also be employed. Mendelian inheritance (or Mendelian genetics or Mendelism) is a set of primary tenets relating to the transmission of hereditary characteristics from parent organisms to their children.

Mendel’s Laws:

Law of segregation:

The “Law of Segregation”, also known as Mendel’s first Law essentially has three parts:

1. Alternative versions of genes account for variations in inherited characteristics:

This is the concept of alleles. Alleles are different versions of genes that impart the same characteristic. For example, each human has a gene that controls eye color, but there are variations among these genes in accordance with the specific color for which the gene ‘codes’.

2. For each characteristic, an organism inherits two alleles, one from each parent:

This means that when somatic cells are produced from two alleles, one allele comes from the mother and one from the father. These alleles may be the same (true-breeding organisms/homozygous, ex. W and ‘rr’ in the figure 3 below), or different (hybrids/heterozygous, ex. ‘wr’ in figure 3 below).

3. The two alleles for each characteristic segregate during gamete production:

This means that each gamete will contain only one allele for each gene. This allows the maternal and paternal alleles to be combined in the offspring, ensuring variation. It is often misconstrued that the gene itself is dominant, recessive, co-dominant, or incompletely dom­inant. It is however, the trait or gene product that the allele encodes that is dominant, etc.

Law of independent assortment:

The law of independent assortment, also known as “Law of Inher­itance” or Mendel’s Second Law, states that the inheritance pattern of one trait will not affect the inheritance pattern of another. While his experiments with mixing one trait always resulted in a 3:1 ratio (As shown in figure 1 below) between dominant and recessive phenotypes, his experiments with mixing two traits (di-hybrid cross) showed 9:3:3:1 ratios (As shown in figure 2 below).

But the 9:3:3:1 table shows that each of the two genes are independently inherited with a 3:1 ratio. Mendel concluded that different traits are inherited independently of each other, so that there is no relation, for example, between a cat’s color and tail length. This is actually only true for genes that are not linked to each other.

Independent assortment occurs during meiosis-I in eukaryotic organisms, specifically anaphase-I of meiosis, to produce a gamete with a mixture of the organism’s maternal and paternal chromosomes. Along with chromosomal cross-over, this process aids in increasing genetic diversity by producing novel genetic combi­nations.

Of the 46 chromosomes in a normal diploid human cell, half are maternally derived (from the mother’s egg) and half are paternally derived (from the father’s sperm). This occurs as sexual reproduction involves the fusion of two haploid gametes (the egg and sperm) to produce a new organism having the full complement of chromosomes.

During gametogenesis, the production of new gametes by an adult the normal complement of 46 chromosomes needs to be halved to 23 to ensure that the resulting haploid gamete can join with another gamete to produce a diploid organism. An error in the number of chromo­somes, such as those caused by a diploid gamete joining with a haploid gamete, is termed aneuploidy.

In independent assortment the chromosomes that end up in a newly-formed gamete are randomly sorted from all possible combinations of maternal and paternal chromosomes. Because gametes end up with a random mix instead of a pre-defined “set” from either parent, gametes are therefore considered assorted independently. As such, the gamete can end up with any combination of paternal or maternal chromosomes.

Any of the possible combinations of gametes formed from maternal and paternal chromosomes will occur with equal frequency. For human gametes, with 23 pairs of chromosomes, the number of possibilities is 2:23 or 8,388,608 possible combinations. The gametes will normally end up with 23 chromosomes, but the origin of any particular one will be randomly selected from paternal or maternal chromosomes. This contributes to the genetic variability of progeny.

The reason for these laws is found in the nature of cell nucleus. It is made up of several chromosomes carrying the genetic traits. In a normal cell, each of these chromosomes has two parts, the chromatids. A reproductive cell, which is created in meiosis, usually contains only one of those chromatids of each chromosome.

By merging two of these cells (usually one male and one female), the full set is restored and the genes are mixed. The resulting cell becomes a new embryo. The fact that this new life has half the genes of each parent (23 from mother, 23 from father for total of 46) is one reason for the Mendelian laws.

The second most important reason is the varying dominance of different genes, causing some traits to appear unevenly instead of averaging out (whereby dominant doesn’t mean more likely to reproduce; recessive genes can become the most common, too).

There are several advantages of this method (sexual reproduction) over reproduction without genetic exchange (asexual reproduction):

1. Instead of nearly identical copies of an organism, a broad range of offspring develops, allowing more different abilities and evolutionary strategies.

2. There are usually some errors in every cell nucleus. Copying the genes usually adds more of them. By distributing them randomly over different chromosomes and mixing the genes, such errors will be distributed unevenly over the different children. Some of them will therefore have only very few such problems. This somewhat helps reduce problems with copying errors.

3. Genes can spread faster from one part of a population to another. This is for instance useful if there’s a temporary isolation of two groups. New genes developing in each of the populations don’t get reduced to half when one side replaces the other, they mix and form a population with the advantages of both sides.

4. Sometimes, a mutation (ex. Sickle cell anemia) can have positive side effects (in this case malaria resistance). The mechanism behind the Mendelian laws can make it possible for some offspring to carry the advantages without the disadvantages until further mutations solve the problems.

Mendelian trait:

A Mendelian trait is one that is controlled by a single locus and shows a simple Men­delian inheritance pattern. In such cases, a mutation in a single gene can cause a disease that is inherited according to Mendel’s laws. Examples include Sickle-cell anemia, Tay-Sachs disease, cystic fibrosis and xero­derma pigmentosa.

A disease controlled by a single gene contrasts with a multi-factorial disease, like arthritis, which is affected by several loci (and the environment) as well as those diseases inherited in a non-Mendelian fashion. The Mendelian inheritance in man data-base is a catalog of, among other things, genes in which Mendelian mutants causes disease.

In genetics, dominance describes a specific relationship between the effects of different versions of a gene (alleles) on a trait (phenotype). Animals (including humans) and plants are mostly diploid, with two copies of each gene, one inherited from each parent.

If the two copies are not identical (not the same allele), their combined effect may be different than the effect of having two identical copies of a single allele. But if the combined effect is the same as the effect of having two copies of one of the alleles, we say that allele’s effect is dominant over the other.

For example, having two copies of one allele of the EYCL3 gene causes the eye’s iris to be brown, and having two copies of another allele causes the iris to be blue. But having one copy of each allele leads to a brown iris. Thus the brown allele is said to be dominant over the blue allele (and the blue allele is said to be recessive to the brown allele).

We now know that in most cases a dominance relationship is seen when the recessive allele is defective. In these cases a single copy of the normal allele produces enough of the gene’s product to give the same effect as two normal copies, and so the normal allele is described as being dominant to the defective allele. This is the case for the eye color alleles described above, where a single functional copy of the ‘brown’ allele causes enough melanin to be made in the iris that the eyes appear brown even when paired with the non-melanin- producing ‘blue’ allele.

Dominance was discovered by Mendel, who introduced the use of uppercase letters to denote dominant alleles and lowercase to denote recessive alleles, as is still commonly used in introductory genetics courses (e.g. ‘Bb’ for alleles causing brown and blue eyes). Although this usage is convenient it is misleading, because dominance is not a property of an allele considered in isolation but of a relationship between the effects of two alleles. When geneticists loosely refer to a dominant allele or a recessive allele, they mean that the allele is dominant or recessive to the standard allele.

Geneticists often use the term dominance in other contexts, distinguishing between simple or complete dominance as described above, and other relationships. Relationships described as incomplete or partial dominance are usually more accurately described as giving an intermediate or blended phenotype. The relationship described as co-dominance describes a relationship where the distinct phenotypes caused by each allele are both seen when both alleles are present.

Nomenclature:

Genes are indicated in short-hand by a combination of one or a few letters:

For exam­ple, in cat coat genetics the alleles Mc and mc (for ‘mackerel tabby’) play a prominent role. Alleles producing dominant traits are denoted by initial capital letters; those that confer recessive traits are written with lowercase letters.

The alleles present in a locus are usually separated by a slash ‘/’; in the ‘Mc’ vs ‘mc’ case, the dominant trait is the ‘mackerel-stripe’ pattern, and the recessive one the ‘classic’ or ‘oyster tabby’ pattern, and thus a classical-pattern tabby cat would carry the alleles ‘mc/mc’, whereas a mackerel-stripe tabby would be either ‘Mc/mc’ or ‘Mc/Mc’.

Relationship to other genetics concepts:

Humans have 23 homologous chromosome pairs (22 pairs of autosomal chromosomes and two distinct sex chromosomes, X and Y). It is estimated that the human genome contains 20,000-25,000 genes. Each chromosomal pair has the same genes, although it is generally unlikely that homologous genes from each parent will be identical in sequence.

The specific variations possible for a single gene are called alleles:

For a single eye-color gene, there may be a blue eye allele, a brown eye allele, a green eye allele, etc. Consequently, a child may inherit a blue eye allele from the mother and a brown eye allele from the father. The dominance relationships between the alleles control which traits are and are not expressed.

An example of an autosomal dominant human disorder is Huntington’s disease, which is a neurological disorder resulting in impaired motor function. The mutant allele results in an abnormal protein, contain­ing large repeats of the amino acid glutamine.

This defective protein is toxic to neural tissue, resulting in the characteristic symptoms of the disease. Hence, one copy suffices to confer the disorder. A list of human traits that follow a simple inheritance pattern can be found in human genetics. Humans have several genetic diseases, often but not always caused by recessive alleles.

Punnett square:

The genetic combinations possible with simple dominance can be expressed by a diagram called a ‘Punnett square’. One parent’s alleles are listed across the top and the other parent’s alleles are listed down the left side. The interior squares represent possible offspring, in the ratio of their statistical probability. In an example of flower color, ‘P’ represents the ‘dominant purple-colored allele’ and ‘p’ the ‘recessive white-colored allele’.

If both parents are purple-colored and heterozygous (Pp), the Punnett square for their offspring would be:

In the PP and Pp cases, the offspring is purple colored due to the dominant P. Only in the pp case is there expression of the recessive white-colored phenotype. Therefore, the phenotypic ratio in this case is 3:1, meaning that F2 generation offspring will be purple-colored three times out of four, on average. Dominant alleles are capitalized.

Dominant allele:

Dominant trait refers to a genetic feature that hides the recessive trait in the pheno­type of an individual. A dominant trait is a phenotype that is seen in both the homozygous ‘AA’ and heterozygous ‘Aa’ genotypes. Many traits are determined by pairs of complementary genes, each inherited from a single parent.

Often when these are paired and compared, one allele (the dominant) will be found to effectively shut out the instructions from the other, the recessive allele. For example, if a person has one allele for blood type A and one for blood type O, that person will always have blood type A. For a person to have blood type O, both their alleles must be O (recessive).

When an individual has two dominant alleles (AA), the individual is referred to as homozygous domi­nant; an individual with two recessive alleles (aa) is called homozygous recessive. An individual carrying one dominant and one recessive allele is referred to as heterozygous. A dominant trait when written in a geno­type is always written before the recessive gene in a heterozygous pair. A heterozygous genotype is written Aa, not aA.

Types of Dominances:

Simple dominance or complete dominance:

Consider the simple example of flower color in peas. The dominant allele is purple and the recessive allele is white.

In a given individual, the two corresponding alleles of the chromosome pair fall into one of the three patterns:

i. Both alleles purple (PP)

ii. Both alleles white (pp)

iii. One allele purple and one allele white (Pp)

If the two alleles are the same (homozygous), the trait they represent will be expressed. But if the individual carries one of each allele (heterozygous), only the dominant one will be expressed. The recessive allele will simply be suppressed.

Simple dominance in pedigrees:

Dominant traits are recognizable by the fact that they do not skip generations, as recessive traits do. It is therefore quite possible for two parents with purple flowers to have white flowers among their progeny, but two such white offspring’s could not have purple offspring (although very rarely, one might be produced by mutation). In this situation, the purple individuals in the first generation must have both been heterozygous (carrying one copy of each allele).

Incomplete dominance:

Discovered by Karl Correns, incomplete dominance (sometimes called partial dominance) is a heterozygous genotype that creates an intermediate phenotype. In this case, only one allele (usually the wild type) at the single locus is expressed in a dosage dependent manner, which results in an intermediate phenotype.

A cross of two intermediate phenotypes (monohybrid heterozygotes) will result in the reappearance of both parent phenotypes and the intermediate phenotype. There is a 1:2:1 pheno­type ratio instead of the 3:1 phenotype ratio found when one allele is dominant and the other is recessive. This lets an organism’s genotype be diagnosed from its phenotype without time-consuming breeding tests. The classic example of this is the color of carnations.

R is the allele for red pigment. R’ is the allele for no pigment. Thus, RR offspring make a lot of red pigment and appear red. R’R’ offspring make no red pigment and appear white. Both RR’ and R’R offspring make some pigment and therefore appear pink.

Co-dominance:

In co-dominance, neither phenotype is recessive. Instead, the heterozygous individual expresses both phenotypes. A common example is the ABO blood group system.

The gene for blood types has three alleles:

A, B, and i. i causes O type and is recessive to both A and B. The A and B alleles are co-dominant with each other. When a person has both an A and a B allele, the person has type AB blood. When two persons with AB blood type have children, the children can be type A, type B, or type AB.

There is a 1A:2AB:1B phenotype ratio instead of the 3:1 phenotype ratio found when one allele is dominant and the other is recessive. This is the same phenotype ratio found in mattings of two organisms that are heterozygous for incomplete dominant alleles. Ex. Punnett square for a father with A and i, and a mother with B and i-

Dominant negative:

Some gain-of-function mutations are dominant and are called ‘dominant negative’ or antimorphic mutations. Typically, a dominant negative mutation occurs when the gene product ad­versely affects the normal, wild-type gene product within the same cell. This usually occurs if the product can still interact with the same elements as the wild-type product, but block some aspect of its function. Such proteins may be competitive inhibitors of the normal protein functions.

Types:

1. A mutation in a transcription factor that removes the activation domain, but still contains the DNA binding domain. This product can then block the wild-type transcription factor from bind­ing the DNA site leading to reduced levels of gene activation.

2. A protein that is functional as a dimer. A mutation that removes the functional domain, but retains the dimerization domain would cause a dominant negative phenotype, because some fraction of protein dimers would be missing one of the functional domains.

Autosomal Dominant Gene:

Autosomal dominant pedigree chart:

An autosomal dominant gene is one that occurs on an autosomal (non-sex determining) chromosome. As it is dominant, the phenotype it gives will be expressed even if the gene is heterozygous. This contrasts with recessive genes, which need to be homozygous to be expressed.

The chances of an autosomal dominant disorder being inherited are 50% if one parent is heterozygous for the mutant gene and the other is homozygous for the normal, or ‘wild-type’, gene. This is because the offspring will always inherit a normal gene from the parent carrying the wild-type genes, and will have a 50% chance of inheriting the mutant gene from the other parent.

If the mutant gene is inherited, the offspring will be heterozygous for the mutant gene, and will suffer from the disorder. If the parent with the disorder is homozygous for the gene, the offspring produced from mating with an unaffected parent will always have the disorder.

The term vertical transmission refers to the concept that autosomal dominant disorders are inherited through generations. This is obvious when you examine the pedigree chart of a family for a particular trait. Because males and females are equally affected, they are equally likely to have affected the children. Although the mutated gene should be present in successive generations in which there are more than one or two offspring, it may appear that a generation is skipped if there is reduced penetrance.

Autosomal dominant disorders:

1. Achondroplasia

2. Anti-thrombin deficiency

3. Autosomal dominant polycystic kidney disease, ADPKD (Adult-onset)

4. BRCA1 and BRCA2 mutations (Hereditary breast ovarian cancer syndrome)

5. Brugada syndrome

6. Charcot-Marie-Tooth syndrome

7. Ectrodactyly

8. Cleft Chin

9. Ehlers-Danlos syndrome

10. Familial hypercholesterolemia

11. Familial adenomatous polyposis

12. Facioscapulohumeral muscular dystrophy

13. Fatal familial insomnia

14. Fibrodysplasia ossificans progressiva

15. Hereditary hemorrhagic telangiectasia (Osler-Weber-Rendu syndrome)

16. Hereditary spherocytosis

17. Hunting’s disease

18. Hypertrophic cardiomyopathy

19. Kabuki syndrome (potentially)

20. Lactase persistence

21. Malignant hyperthermia

22. Mandibulofacial dysostosis

23. Marfan syndrome

24. Mowat-Wilson syndrome

25. Multiple endocrine neoplasia

26. Noonan syndrome

27. Neurofibromatosis

28. Osteogenesis imperfect

29. Pfeiffer syndrome

30. Tuberous sclerosis

Recessive allele:

The term ‘recessive allele’ refers to an allele that causes a phenotype (visible or detectable characteristic) that is only seen in homozygous genotypes (organisms that have two copies of the same allele) and never in heterozygous genotypes.

Every diploid organism, including humans, has two copies of every gene on autosomal chromosomes, one from the mother and one from the father. The dominant allele of a gene will always be expressed while the recessive allele of a gene will be expressed only if the organism has two recessive forms. Thus, if both parents are carriers of a recessive trait, there is a 25% chance with each child to show the recessive trait.

The term ‘recessive allele’ is part of the laws of Mendelian inheritance formulated by Gregor Mendel. Examples of recessive traits in Mendel’s famous pea plant experiments include the color and shape of seed pods and plant height.

Autosomal recessive allele:

Autosomal recessive is a mode of inheritance of genetic traits located on the autosomes (the pairs of non-sex determining chromosomes—22 in humans).

In opposition to autosomal dominant trait, a recessive trait only becomes phenotypically apparent when two similar alleles of a gene are present. In other words, the subject is homozygous for the trait.

The frequency of the carrier state can be calculated by the Hardy-Weinberg formula:

p² + 2pq + q² = 1 (p is the frequency of one pair of alleles, and q = 1 – p is the frequency of the other pair of alleles).

Recessive genetic disorders occur when both parents are carriers and each contributes an allele to the embryo, meaning these are not dominant genes. As both parents are heterozygous for the disorder, the chance of two disease alleles landing in one of their offspring is 25% (in autosomal dominant traits this is higher).

50% of the children (or 2/3 of the remaining ones) are carriers. When one of the parents is homozygous, the trait will only show in his/her offspring if the other parent is also a carrier. In that case, the chance of disease in the offspring is 50%.

Nomenclature of recessiveness:

Technically, the term ‘recessive gene’ is imprecise because it is not the gene that is recessive but the phenotype (or trait). It should also be noted that the concepts of recessiveness and dominance were developed before a molecular understanding of DNA and before development of molecular biology, thus mapping many newer concepts to ‘dominant’ or ‘recessive’ phenotypes is prob­lematic.

Many traits previously thought to be recessive have mild forms or biochemical abnormalities that arise from the presence of one copy of the allele. This suggests that the dominant phenotype is dependent upon having two dominant alleles, and the presence of one dominant and one recessive allele creates some blending of both dominant and recessive traits.

Mendel performed many experiments on pea plant (Visum sativum) while researching traits, chosen because of the simple and low variety of characteristics, as well as the short period of germination. He experimented with color (‘green’ vs. ‘yellow’), size (‘short’ vs. ‘tall’), pea texture (‘smooth’ vs. ‘wrinkled’), and many others. By good fortune, the characteristics displayed by these plants clearly exhibited a dom­inant and a recessive form. This is not true for many organisms.

For example, when testing the color of the pea plants, he chose two yellow plants, since yellow was more common than green. He mated them, and examined the offspring. He continued to mate only those that appeared yellow, and eventually, the green ones would stop being produced. He also mated the green ones together and determined that only green ones were produced.

Mendel determined that this was because green was a recessive trait which only appeared when yellow, the dominant trait, was not present. Also, he determined that the dominant trait would be displayed whether or not the recessive trait was there.

Autosomal recessive disorders:

Dominance/recessiveness refers to phenotype, not genotype. An ex­ample to prove the point is sickle cell anemia. The sickle cell genotype is caused by a single base pair change in the beta-globin gene, normal is GAG (glu) and sickle is GTG (val).

There are several phenotypes associated with the sickle genotype:

1. Anemia (a recessive trait)

2. Blood cell sickling (co-dominant)

3. Altered beta-globin electrophoretic mobility (co-dominant)

4. Resistance to malaria (dominant)

This example demonstrates that one can only refer to dominance/recessiveness with respect to individual phenotypes.

Other recessive disorders:

1. Albinism

2. Alpha 1-antitrypsin deficiency

3. Autosomal Recessive Polycystic Kidney

4. Bloom’s syndrome

5. Certain forms of spinal muscular atrophy

6. Chronic granulomatous disease

7. Congenital adrenal hyperplasia deficiency

8. Cystic fibrosis

9. Dry (also known as ‘rice-bran’) earwax

10. Dubin-Johnson syndrome

11. Familial Mediterranean fever Disease-ARPKD (Child-onset)

12. Fanconi anemia

13. Friedreich’s ataxia

14. Galactosemia

15. GluC0SC-6-ph0Sphate dehydrogenase

16. Glycogen storage diseases

17. Haemochromatosis types 1-3

18. Homocystinuria

19. Mucopolysaccharidoses

20. Pendred syndrome

21. Phenylketonuria

22. Rotor syndrome

23. Tay-Sach’s disease

24. Thalassemia

25. Wilson’s disease

26. Xeroderma pigmentosum

Mechanisms of dominance:

Many genes code for enzymes. Consider the case where someone is ho­mozygous for some trait. Both alleles code for the same enzyme, which causes a trait. Only a small amount of that enzyme may be necessary for a given phenotype.

The individual therefore has a surplus of the necessary enzyme. Let’s call this case ‘normal’. Individuals without any functional copies cannot produce the enzyme at all, and their phenotype reflects that. Consider a heterozygous individual. Since only a small amount of the normal enzyme is needed, there is still enough enzyme to show the phenotype. This is why some alleles are dominant over others.

In the case of incomplete dominance, the single dominant allele does not produce enough enzymes, so the heterozygotes show some different phenotype. For example, fruit color in eggplants is inherited in this manner.

A purple color is caused by two functional copies of the enzyme, with a white color resulting from two non-functional copies. With only one functional copy, there is not enough purple pigment, and the color of the fruit is a lighter shade, called violet.

Some non-normal alleles can be dominant. The mechanisms for this are varied, but one simple example is when the functional enzyme E is composed of several subunits where each Ei is made of several alleles Ei = ailai2, making them either functional or not functional according to one of the schemes described above.

For example one could have the rule that if any of the Ei subunits are non-functional, the entire enzyme E is non-functional in the sense that the phenotype is not displayed. In the case of a single subunit say El is El = F where F has a functional and non-functional allele (heterozygous individual) (F = a1A1), the concentration of functional enzyme determined by E could be 50% of normal. If the enzyme has two identical subunits (the concentration of functional enzyme is 25% of normal).

For four subunits, the concentration of functional enzyme is about 6% of normal (roughly scaling slower than 1/2c where c is the number of copies of the allele-1/24 is about 51% percent). This may not be enough to produce the wild type phenotype. There are other mechanisms for dominant mutants.

Sex-limited genes:

Sex-limited genes are genes which are present in both sexes of sexually reproducing species but turned on in only one sex. In other words, sex-limited genes cause the two sexes to show different traits or phenotypes. An example of sex-limited genes are genes which instructs male elephant seal to grow big and fight, at the same time instructing female seals to grow small and avoid fights. These genes are responsible for sexual dimorphism.