The mutant gene might cause the generation of an altered protein that interfered in some reaction with the cell and thus caused a deleterious phenotype. In this case, the presence of a wild-type allele would restore the function missing in the mutant but would not eliminate the deleterious phenotype caused by the mutant protein. Thus, the mutant phenotype would be dominant to wild type. In each case, an altered product is responsible for the trans dominance. Such trans -dominant mutants are very appropriate for further biochemical analysis because the protein product has alteredfunction, rather than merely a lack of function.
Intragenic complementation is yet another possible complication in complementation analysis.
This term refers to cases where two mutations that do affect the same gene, and therefore the same gene product, are able nonetheless to give a wild-type phenotype in a complementation analysis. If two such mutations were put in a merodiploid situation, each would be able to produce one of the two required enzymatic functions, giving rise to a wild-type phenotype. In the case of such a gene, intragenic complementation would be fairly common such that many mutations would affect only one of the two functional regions. This model also predicts that mutations affecting each of the two functions would cluster at either end of the gene creating two clear complementation groups. In such cases, a particular mutant allele might give rise to a protein product that can only function when allowed to aggregate with another particular mutant allele.