FIGURE 4 | Models of non-allelic complementation.

From the following article:

Beyond Mendel: an evolving view of human genetic disease transmission

Jose L. Badano & Nicholas Katsanis

Nature Reviews Genetics 3, 779-789 (October 2002)

doi:10.1038/nrg910

Beyond Mendel: an evolving view of human genetic disease transmission

a, b | The direct-interaction dosage model. a | Mutations at one locus (mutated proteins are indicated by asterisks) are not sufficient to disrupt the formation of the complex between proteins A and B, although the strength of the interaction might be reduced (dashed line). A further mutation in protein B causes disruption of the complex (red cross), resulting in a detectable phenotype. b | A similar model involving proteins B and D, which are members of the same multi-subunit complex but do not interact directly. c | The poison model. Mutations in protein A disrupt the complex, although enough functional units remain to maintain function. A further mutation (or mutations) in protein D disrupts more units, resulting in the disruption of a physiological process and the generation of a cellular phenotype.

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