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Therefore no trait is purely Mendelian, but many traits are almost entirely Mendelian, including canonical examples, such as those listed below. Purely Mendelian traits are a minority of all traits, since most phenotypic traits exhibit incomplete dominance, codominance, and contributions from many genes.
In cases of intermediate inheritance due to incomplete dominance, the principle of dominance discovered by Mendel does not apply.Nevertheless, the principle of uniformity works, as all offspring in the F 1-generation have the same genotype and same phenotype.
Very few phenotypes are purely Mendelian traits. Common violations of the Mendelian model include incomplete dominance, codominance, genetic linkage, environmental effects, and quantitative contributions from a number of genes (see: gene interactions, polygenic inheritance, oligogenic inheritance). [1] [2]
Co-dominance, where allelic products co-exist in the phenotype, is different from incomplete dominance, where the quantitative interaction of allele products produces an intermediate phenotype. For example, in co-dominance, a red homozygous flower and a white homozygous flower will produce offspring that have red and white spots.
Compared to examples of overdominance in actual populations, underdominance is considered more unstable [3] [4] and may lead to the fixation of either allele. [ 1 ] [ 5 ] [ 6 ] An example of stable underdominance may occur in individuals who are heterozygotic for polymorphisms that would make them better suited for one of two niches . [ 7 ]
Pseudodominance is the situation in which the inheritance of a recessive trait mimics a dominant pattern. [1]Normally, two recessive alleles need to be inherited (one from each parent) for the recessive trait to be expressed but recessive merely means that the trait is only expressed in the absence of the dominant alleles.
[7] [8] In 2014, there were about 150 imprinted genes known in mice and about half that in humans. [9] As of 2019, 260 imprinted genes have been reported in mice and 228 in humans. [10] Genomic imprinting is an inheritance process independent of the classical Mendelian inheritance. [11]
An example of this is seen in the case of Williams syndrome, a neurodevelopmental disorder caused by the haploinsufficiency of genes at 7q11.23. The haploinsufficiency is caused by the copy-number variation (CNV) of 28 genes led by the deletion of ~1.6 Mb. These dosage-sensitive genes are vital for human language and constructive cognition. [2]