Complementation (genetics)

Complementation refers to a genetic process when two strains of an organism with different homozygous recessive mutations that produce the same mutant phenotype (for example, a change in wing structure in flies) have offspring that express the wild-type phenotype when mated or crossed.

[2][3] The complementation test was one of the main tools used in the early Neurospora work, because it was easy to do, and allowed the investigator to determine whether any two nutritional mutants were defective in the same or different genes.

The complementation test was also used in the early development of molecular genetics when bacteriophage T4 was one of the main objects of study.

[4] In this case the test depends on mixed infections of host bacterial cells with two different bacteriophage mutant types.

Its use was key to defining most of the genes of the virus, and provided the foundation for the study of such fundamental processes as DNA replication and repair, and how molecular machines are constructed.

Heterosis appears to be largely due to genetic complementation, that is the masking of deleterious recessive alleles in hybrid individuals.

Outcrossing is proposed to be adaptive because it facilitates complementation, that is the masking of deleterious recessive alleles [5] (also see heterosis).

The benefit of masking deleterious alleles has been proposed to be a major factor in the maintenance of sexual reproduction among eukaryotes.

Transvection is another instance, in which a heterozygous combination of two alleles with mutations in distinct sections of the gene complement one other to restore a wild-type phenotype.

An analysis of the results from such studies led to the conclusion that intragenic complementation, in general, arises from the interaction of differently defective polypeptide monomers to form an aggregate called a “multimer.”[9] Genes that encode multimer-forming polypeptides appear to be common.

Example of a complementation test. Two strains of flies are white-eyed because of two different autosomal recessive mutations that interrupt different steps in a single pigment-producing metabolic pathway. Flies from Strain 1 have complementary mutations to flies from Strain 2 because when they are crossed the offspring can complete the full metabolic pathway and thus have red eyes.