Codominance – Not Always the Best of Both Worlds

Within this past unit of study, we focused largely on patterns of inheritance. Inheritance can be defined as the process by which genetic information is passed on from the parents to their offspring. One of the most basic principles of inheritance is known as Mendel’s law of dominance. This law states that if two alleles at a locus differ, then one, the dominant allele, determines the organism’s appearance; the other, the recessive allele, has no noticeable effect on the organism’s appearance. Dominant alleles are not necessarily better or stronger than recessive alleles, nor do they necessarily occur more often in a population. An allele is “dominant” in a heterozygote simply because it is expressed and the recessive allele is not. There are some exceptions to this law however.

One common relationship between two versions of a gene that does not necessarily follow this law is known as codominance. With codominance, both alleles are expressed completely; neither allele is dominant or recessive and both traits are sully and separately expressed. Codominance can also occur in traits that may be less visible, like blood type. Within this, the A and B alleles for blood type can both be expressed at the same time, which results in type AB blood.

Blood Type Codominance
This figure shows the codominant relationship of the ABO blood type genotype and phenotype.
Image from Wikimedia Commons

Another prime example of codominance involves alpha-1 antitrypsin (AAT), a protein made within the liver. The liver releases this AAT into the bloodstream in order to protect the lungs so they can function properly. Without enough of this protein, the lungs can be damaged which may make breathing much more difficult. Alpha-1 antitrypsin deficiency (AATD) is an inherited condition that either causes low levels of alpha-1 antitrypsin (AAT) in the blood or none at all. Therefore, this deficiency raises one’s genetic risk for getting both lung and liver failure.

Everyone has two copies of the gene for AAT, one copy inherited from each parent. Most people have two normal copies of the alpha-1 antitrypsin gene. However, individuals with this deficiency have one normal copy and one damaged copy, or they have two damaged copies. Alpha-1 antitrypsin deficiency is known to be inherited in an autosomal codominant pattern. Within this malady, there are three different alleles possible for this particular gene. The M gene produces normal levels of the alpha-1 antitrypsin protein, and is the most common allele of the alpha-1 gene. The Z gene is the most common variant of the gene that causes alpha-1 antitrypsin deficiency, and the S allele is another although less common. If a person inherits a heterozygous genotype (one M gene and one Z gene or one S gene), they will be a carrier of the disorder. While they may not have normal levels of alpha-1 antitrypsin, there would most likely be enough of this protein to protect the lungs.

Typically, codominance is associated with either blood type and a variety of more visible phenotypes, such as the fur color of a certain animal, however this pattern of inheritance is actually more harmful in the case of AATD. With a heterozygous genotype, there are still proteins present, although not as many as what is considered normal, and therefore still generating a risk of lung and liver diseases. For this reason, the National Human Genome Research Institute concludes that AATD is inherited through autosomal codominance, rather than another pattern of inheritance such as incomplete dominance. The effects of this disorder present differently depending on the person as well as their environmental risk factors. Although someone with a homozygous recessive genotype may be at a very high risk of lung and/or liver disease, it is not guaranteed they will develop either in the future. Presenting both phenotypes in this codominant pattern is a major disadvantage in this case, more like the deficiency itself.

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Biology Teacher

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