Non-Mendelian Genetics: Introduction, Overview, And Its Various Types of Dominance

Non-Mendelian Genetics Introduction

Since Mendel’s time, scientists have discovered a variety of Non-Mendelian Genetics that alter offspring’s genotypic and phenotypic ratios. In the previous section, we looked at how Mendel’s Laws of Inheritance enable us to anticipate how unrelated characteristics with perfect dominance are inherited. In most species, however, there are just a few features that have total dominance and are unrelated to other traits.

We’ll examine partial dominance and codominance in this section, comparing them to total dominance. Then we’ll examine how linkage (connected genes) might cause the Law of Independent Assortment to be broken. We’ll also look at how a single gene may influence numerous characteristics (pleiotropy) and how multiple genes can influence a single trait (multiple genes) (polygenic trait). Finally, we’ll discuss sex-related genes, deadly alleles, and non-nuclear inheritance (mtDNA and chloroplast DNA).

Non-Mendelian Genetics Overview

Did you know that you are biologically linked to your mother more than you are to your father? While your parents both supplied an equal number of chromosomes, your mother provided all of your mitochondria and the mitochondrial DNA they contained. Because the mitochondria in sperm cells are eliminated after conception, mitochondria can only be inherited via egg cells.

Non-Mendelian genetics may give even more diversity and complexity to living creatures, whereas standard ways of Mendelian inheritance can redistribute features and variations. Different types of dominance, such as codominance and incomplete dominance, and linked genes, which are not inherited totally independently of one another, are examples of non-Mendelian genetics.

They also contain genes that influence several characteristics and traits that are influenced by multiple genes. There are additional organelles such as mitochondria and chloroplasts that have their own DNA and are inherited in a different way than conventional chromosomes. Non-Mendelian genetics will undoubtedly be on the AP exam. So bear with us as we give you a fast rundown of all you need to know about Non-Mendelian Genetics.

So, what does “Non-Mendelian” genetics entail? This phrase refers to features and genes that do not follow Mendel’s principles of inheritance. Non-Mendelian genetics refers to any characteristic in which alleles do not demonstrate total dominance or are inherited in unusual ways. Watch our prior video on section 5.3 if you need a refresher on normal Mendelian genetics.

Incomplete dominance

Let’s start with two types of non-Mendelian genetics that deal with different types of dominance. When the heterozygote for a specific characteristic has a combination of both homozygous phenotypes, this is known as incomplete dominance. If a red homozygous flower and a white homozygous bloom both have inadequate dominance on alleles, the hybrid will resemble neither of the parents—in this situation, a pink flower will result. The alleles are commonly labelled with a superscript – “AR” for the red allele and “AW” for the white allele – since neither is dominant in the hybrid.

Here’s what’s probably going on at the molecular level. Each allele results in a unique variant of the same protein. In this hypothetical scenario, the red allele’s protein converts a white pigment molecule into a red pigment molecule at the conclusion of a complicated pigment manufacturing process. The non-functional protein produced by the alternative white allele just passes the white pigment through. When an organism possesses both alleles, it generates equal quantities of white and red pigment molecules, resulting in a pink flower.

Complete dominance

A very similar molecular scenario might arise in normal Mendelian full dominance. Complete dominance, on the other hand, entirely conceals the recessive gene in the heterozygous phenotype. This might be because the dominant allele’s pigment molecule is powerful enough to overwhelm the white pigment molecule even when it is present in small proportions.


Let us now discuss codominance. The heterozygote does not have a distinct phenotype from both homozygotes in codominant characteristics. Rather, the heterozygote manifests both homozygous and heterozygous traits. The AB blood type is a prominent example of codominance. Blood type-A, B, and O-is another example of a characteristic having numerous alleles. The A and B alleles have traditionally dominated the O allele. When A and B are present in the same cell, however, both genes are expressed.

This is what is going on at the cellular level. The O allele causes a non-functional cell-surface protein to be produced that never reaches the cell membrane. Different functional variants of these membrane proteins are produced by the A and B alleles. Because both alleles are present, both proteins reach the cell surface, creating A and B codominant alleles.

It’s also worth noting that these genes are not inherited in the same proportions as totally dominant features since they don’t obey Mendel’s principles. These other kinds of dominance, however, are not the only sorts of genetics that defy Mendel’s principles!

Consider this… Mendel was fortunate in that he began his genetic studies on a purebred line of pea plants and selected the features that he did. Many additional pea plant features, like those of other plants, are determined by non-Mendelian laws. For example, the colour of lentils is controlled by several genes, which would have been far more difficult for Mendel to figure out!

Linkage is one of the most prevalent breaches of Mendel’s rules, which occurs when two genes on the same chromosome are not inherited fully separately. This is significantly more prevalent than Mendel’s principles should predict, given that humans have over 22,000 genes and just 23 chromosomes.

To understand how connected genes might throw off Mendelian inheritance ratios, we must first understand how chromosomes are separated. Remember that each homologous chromosome has identical genes, and each sister chromatid has a copy of each gene’s allele. During meiosis, each of these sister chromatids will be split into distinct gametes. While genes on distinct chromosomes may be inherited separately, alleles for the same chromosome are often found in the same gamete.

Crossing over may be used to segregate alleles on the same sister chromatid, although it works best when genes are spread out across a chromosome. This technique successfully blends alleles from homologous chromosomes, giving the impression that two qualities are unrelated.

When genes are relatively close to one another, however, the act of crossing over seldom separates them. While some alleles cross over, closely related alleles are nearly always inherited together. In fact, related genes may aid in the mapping of distinct genes on a chromosome.

We may estimate how near two genes are situated on a chromosome by comparing the frequency with which two characteristics are found together in a group of children. If we measure the frequency with which eye colour and blood type are inherited jointly, we may obtain a figure of about 60%. If we measure hair colour and eye colour, we may obtain a percentage of 10%.

We know these features are all on the same chromosome because we know there is at least some connection between them. However, we know that eye colour and blood type are more closely related since they are inherited together more often. The process of crossing across separates genes that are closer together less often. As a result, we can effectively map a chromosome based on the distance between particular connected genes!

Now we’ll briefly go through a few other kinds of inheritance that don’t follow the traditional Mendelian ratios. Let’s start with polygenic characteristics, which are features that are regulated by numerous genes. Because there are so many distinct genes at play, polygenic characteristics are not inherited in the traditional Mendelian ratios. Human skin colour is a superb example of a polygenic characteristic. Similar to height, weight, and eye colour, skin colour is regulated by numerous genes inside the human genome and occurs on a sliding spectrum between two extremes.

Pleiotropy is a non-Mendelian pattern of inheritance in which one gene is responsible for numerous, apparently unrelated features. Consider a chicken gene that causes the feathers to be considerably more frizzy than they should be. This gene boosts the chicken’s hunger, heart rate, and even delays sexual maturity, which is unusual. All of these things are tied to the frizzy gene, which codes for the same protein in chickens.

When lethal alleles are implicated, several unusual phenotypic ratios emerge. When lethal alleles are inherited, they are deadly. Lethal alleles may be dominant (as in Huntington’s disease) or recessive (as is the case with cystic fibrosis). When deadly alleles cause embryonic death, researchers seldom see the children. As a result, the offspring’s phenotypic ratio may be dramatically influenced—statistically suggesting a deadly gene is certainly implicated.

Finally, sex-related features (not to be confused with linked genes) should be considered. Any characteristic regulated by any of the genes on the sex chromosomes is referred to as a sex-linked trait (X and Y in humans). Because females have two X chromosomes and males have one X and one Y, sex-linked features change Mendelian ratios. The X and Y chromosomes carry distinct genetic material from the other maternal and paternal chromosomes in the cell, which have homologs containing the same genes.

A sex-linked recessive condition passed down from the mother, for example, may result in carrier females, afflicted males, unaffected females, and unaffected males. Male kids are never impacted if the father is the carrier, since they never acquire an X from the father. Affected fathers, on the other hand, always produce carrier daughters because they must inherit the affected X chromosome. These are only a few examples of how phenotypic ratios are affected by sex-linked variables! If you come across any of these odd forms of inheritance on the exam, be sure to use a Punnett square!

The last mechanism of non-Mendelian inheritance is concerned with DNA that is not found in the nucleus. The DNA contained in chloroplasts and mitochondria, in particular, still contains vital genetic information. On the other hand, these types of DNA,  are not handed on to the next generation in the same way that nuclear DNA is.

Non-nuclear inheritance

Though sperm cells include mitochondria, which supply energy to the cell, these mitochondria are not transmitted to the egg cell during fertilisation. Non-nuclear inheritance is the term for this.

The sperm cell just gives the new zygote its nucleus and discards the remainder of the cell. As a result, a zygote’s only mitochondria are those that were previously present in the egg cell. These mitochondria will multiply themselves by binary fission when the zygote divides, and will be randomly assigned to each new cell.

As a result, unlike standard Mendelian genetics, mitochondrial and chloroplast DNA inheritance has no paternal component. You obtain fragments of DNA from all of the people in your family who came before you through regular Mendelian inheritance. Mitochondria, on the other hand, exclusively migrate down the maternal line. As a result, geneticists may use your mitochondrial DNA and the changes it contains to track your mother line (also known as a maternal haplogroup) all the way back to the origin of mankind.

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