incomplete. The important thing to remember about dominance is that it affects the phenotype that genes produce, but not the way in which genes are inherited.

Another type of interaction between alleles is codomi-nance, in which the phenotype of the heterozygote is not intermediate between the phenotypes of the homozygotes; rather, the heterozygote simultaneously expresses the phe-notypes of both homozygotes. An example of codominance is seen in the MN blood types.

The MN locus codes for one of the types of antigens on red blood cells. Unlike antigens foreign to the ABO and Rh blood groups (which also code for red-blood-cell antigens), foreign MN antigens do not elicit a strong immunological reaction, and therefore the MN blood types are not routinely considered in blood transfusions. At the MN locus, there are two alleles: the LM allele, which codes for the M antigen; and the LN allele, which codes for the N antigen. Homozygotes with genotype LMLM express the M antigen on their red blood cells and have the M blood type. Homozygotes with genotype LNLN express the N antigen and have the N blood type. Heterozygotes with genotype LMLN exhibit codominance and express both the M and the N antigens; they have blood type MN. The differences between dominance, incomplete dominance, and codominance are summarized in Table 5.1.

The type of dominance that a character exhibits frequently depends on the level of the phenotype examined. An example is cystic fibrosis, one of the more common genetic disorders found in Caucasians and usually considered to be a recessive disease. People who have cystic fibrosis produce large quantities of thick, sticky mucus, which plugs up the airways of the lungs and clogs the ducts leading from the pancreas to the intestine, causing frequent respiratory infections and digestive problems. Even with medical treatment, patients with cystic fibrosis suffer chronic, life-threatening medical problems.

The gene responsible for cystic fibrosis resides on the long arm of chromosome 7. It encodes a protein termed cystic fibrosis transmembrane conductance regulator, mercifully abbreviated CFTR, which acts as a gate in the cell membrane and regulates the movement of chloride ions into and out of the cell. Patients with cystic fibrosis have a mutated, dysfunctional form of CFTR that causes the channel to stay closed, and so chloride ions build up in the cell. This buildup causes the formation of thick mucus and produces the symptoms of the disease.

Most people have two copies of the normal allele for CFTR, and produce only functional CFTR protein. Those with cystic fibrosis possess two copies of the mutated CFTR allele, and produce only the defective CFTR protein. Heterozygotes, with one normal and one defective CFTR allele, produce both functional and defective CFTR protein. Thus, at the molecular level, the alleles for normal and defective CFTR are codominant, because both alleles are expressed in the heterozygote. However, because one normal allele produces enough functional CFTR protein to allow normal chloride transport, the heterozygote exhibits no adverse effects, and the mutated CFTR allele appears to be recessive at the physiological level.

In summary, several important characteristics of dominance should be emphasized. First, dominance is a result of interactions between genes at the same locus; in other words, dominance is allelic interaction. Second, dominance does not alter the way in which the genes are inherited; it only influences the way in which they are expressed as a phenotype. The allelic interaction that characterizes dominance is therefore interaction between the products of the genes. Finally, dominance is frequently "in the eye of the beholder," meaning that the classification of dominance depends on the level at which the phenotype is examined. As we saw with cystic fibrosis, an allele may exhibit codomi-nance at one level and be recessive at another level.

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