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An example often stated for codominance is blood groups, where both alleles version of the protein is expressed and can be found in the cell membrane.

An example of incomplete dominance often given is of red and white flowered snapdragons giving pink flowered offspring because enzymes for both pigments are transcribed and translated and the mixing of these pigments gives the intermediate phenotype.

In both these examples both alleles are transcribed and translated.

In the text-book mendelian situation of a dominant and recessive allele are there actually a cellular mechanisms by which a 'dominant' allele silences the 'recessive' allele and inhibits it's translation, transcription or both? If so are there any well characterised examples?

Or are all alleles actually codominant at the transcription/protein level? e.g like in many recessive gentic diseases where both the mutant and the normal protein are present (cystic fibrosis, sickle cell anemia etc) but the activity of the normal protein gives the 'healthy' phenotype.

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  • $\begingroup$ Related: Evolution of dominance of alleles $\endgroup$ – Remi.b Apr 21 at 19:19
  • $\begingroup$ I don't think dominance is subjective at all. Do you have any references for the claims you made? For example "for a physician the healthy allele is dominant". $\endgroup$ – Cell Apr 21 at 19:26
  • $\begingroup$ As @Cell said, you seem to confound dominance with fitness. Make sure to clarify that. Many people also confound dominance and frequency. Make sure to understand that these concepts are very different. $\endgroup$ – Remi.b Apr 21 at 19:31
  • $\begingroup$ @Cell I'll reword the question but I am paraphrasing from an example in my undergrad lectures $\endgroup$ – Mirte Apr 21 at 20:28
  • $\begingroup$ @Mirte It is a good question +1. Can you please make sure to cite your source (what text-book are you referring to) and eventually give a direct quote (although you don't necessarily have to). $\endgroup$ – Remi.b Apr 21 at 21:42
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"Or are all alleles actually codominant at the transcription/protein level?"

Yes this is the right idea. Generally all alleles are transcribed independently (with some exceptions like in females where one X chromosome is inactivated). And the dominant and recessive phenotypes are in a sense extreme cases of codominance. The terms are used for describing phenotypes and depend on thresholds of activity. In the snapdragons example we can associate 2 functional enzymes EE with the red phenotype and white (lack of red pigment) associated with 2 nonfunctional enzymes ee. But one E is not enough to make the red pigment so we see some red pigment and a pink phenotype.

Now consider a yeast cell with 2 hexokinase genes (H). With two inactive proteins (h/h), the cell will grow slowly. Now let's say that H is a very efficient protein and that glucose transport into the cell is rate limiting so one active H has the same phenotype as having 2 H/H, so H/H is the same as H/h thus H is a dominant allele and h is recessive because one H is past the threshold of activity for fast growth on glucose. h is recessive because h/h genotype is needed to see the h phenotype. Hope that helps.

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An example of incomplete dominance often given is of red and white flowered snapdragons giving pink flowered offspring because enzymes for both pigments are transcribed and translated and the mixing of these pigments gives the intermediate phenotype.

White snapdragons are not making a white pigment. A step in the pigment-making pathway fails, because a needed gene is broken. A snapdragon with one working pigment enzyme allele makes some pigment, but not as much as one with two working enzyme alleles.

https://en.wikipedia.org/wiki/Haploinsufficiency

A blood does not react to A blood. B blood does not react to B blood. AB blood doesn't react to A or B blood.

One copy of the A allele does all the same stuff as having two copies. One copy of a working pigment enzyme does not make as much pigment as two working copies.

In both these examples both alleles are transcribed and translated.

It is not at all clear to me that the broken pigment enzyme is necessarily translated at the same rate as the working one. There are cellular mechanisms to clear away non-functional transcripts, the broken enzyme transcript might be subject to those processes.

https://en.wikipedia.org/wiki/Nonsense-mediated_decay

Or the defect in the broken allele might be in its promoter, preventing it from being transcribed at all.

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