Going back to my high school days we were taught about dominant and recessive genes. We were taught how to calculate the geneotype and pheneotype of potential offspring using a small table (forgotten the actual table name). But it never occurred to me then what determines if a gene is dominant or recessive and how this is carried out biologically.

Take my example below, there is a 50% change that an offspring will carry both the tall (T) and short (t) genes. What determines that the tall gene T has a dominant effect over the short gene t.

Now, I know that there is going to be differences between the different genes (i.e. eye colour), but is there a general description any one and provide which states how a gene becomes dominant and how the dominant effect is carried out biologically.

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    $\begingroup$ A common cause is haplosufficiency, i.e. that a single copy of an allele will produce enought protein to create a heterozygote phenotype that is similar to the homozygote phenotype. $\endgroup$ – fileunderwater Oct 22 '13 at 11:08
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    $\begingroup$ Which "why" are you asking? Do you mean "Why" like "why did it evolve that there is dominance rather that additivity?" or "why" like "what genetic mechanisms creates a relation of dominance between two alleles?" $\endgroup$ – Remi.b Oct 22 '13 at 15:15
  • $\begingroup$ If "why" meant "what evolutionary reasons" then, there are maybe two models that are worth talking about which are Fisher's model and Wright's model of the evolution of dominance $\endgroup$ – Remi.b Oct 22 '13 at 15:18
  • $\begingroup$ An interesting example I like is that horns on cattle is recessive, but having horns gives enough of an advantage that the trait became very common. But if you have a bull with two copies of the dominant no horns allele, none of your calves will have horns. Just an example that recessive traits aren't always rarer in nature. $\endgroup$ – user137 Apr 28 '15 at 1:31

Dominance is seldom complete. Owing to effects like co-dominance, incomplete dominance, collaborative (additive) effects of polygenes, our classical concept of dominance doesn't work. Having said that, there are certain ways in which a gene, if showing complete dominance can be analysed from the molecular level.

In an individual heterozygous for a certain trait, the following possibilities exist:

  1. Both the alleles, though different, code for a protein (which might be an enzyme or a regulatory protein) which is functional and is indistinguishable atleast in terms of its functions. In this case, no matter if the person is heterozygous or homozygous for either allele, the concerned protein will be in sufficient amounts and will always be functional. These alleles can be treated as the same allele while performing Mendelian analysis though their products might differ slightly, leading to formation of two (or more) functionally similar Alloenzymes (as opposed to Isozymes which are similar enzymes produced by genes at different loci).

  2. Haplosufficiency. In this case, one of the two alleles codes for a functional protein and the other either codes for a non-functional protein (or does not code at all). But, even in heterozygous condition where only one allele producing functional protein is present, the amount of protein produced is sufficient to show the phenotype and hence, even in heterozygous individuals, enough protein is coded for by the single functional allele exhibiting the normal phenotype. If the two non-functional alleles are present as a homozygous pair, no functional protein is synthesised and hence the phenotype is not shown (i.e a different phenotype is shown). Here, the functional allele is Haplosufficient (able to produce enough protein in heterozygous condition) and is called the dominant since it expresses its phenotype both in heterozygous and homozygous conditions. this is pretty common.

  3. Complete Haploinsufficiency. Here again one allele codes for a functional protein while the other does not. But this time, if the functional allele is present in heterozygous condition, then the amount of the protein produced is not at all sufficient and hence the phenotype is not exhibited. Here the non-functional allele is said to be dominant because heterozygous phenotype resembles the phenotype of homozygous non-functional allele (where no protein is synthesized) since the functional allele is completely haploinsufficient (unable to produce enough protein in heterozygous condition). This method is pretty rare.(e.g rare autosomal dominant dyskeratosis congenita)

If there is partial haplosufficiency /partial haploinsufficiency, the phenomenon of incomplete dominance can be explained. (heterozygous individual produces protein not sufficient for a full-blown phenotype but just a partial expression of the phenotype)

Here, "functional" refers to being actually "functional" as in case of flower colour (anthocyanin synthesis) or just performing certain kind of a conversion leading to a particular effect on thephenotype.


Fisher and Wright provided two different models in order to explain why newly arisen mutations tend to be recessive. I am not sure though if this answer your question!

Fisher's model

"...there is a tendency always at work in nature which modifies the response of the organism to each mutant gene in such a way that the wild type tends to become dominant." Given that most mutations are deleterious, there is selection to make fixed mutations dominant over almost any mutations that could appear.

Wright's model

"...mutations are most frequently in the direction of inactivation and that for physiological reasons inactivation should generally behave as recessive."

There are 2 physiological reasons.

1) Deleterious mutations are mutations that usually cause a protein to not work properly. Given that the kinetics of reaction is usually not linear but is a function which derivative is decreasing over the number of enzyme, if we divide by 2 the number of functionning protein, we divide by less than two the reaction rate. Therefore, a deleterious mutation is usually recessive.

2) The reagents of a given reaction are often the products of another one. If this other reaction is slow compare to the reaction that followed, diminishing the rate the following reaction will not have a big impact on the rate of the overall metabolic pathway. Therefore, most deleterious mutations are recessive.

More information here

Note that there is a correlation between the impact a mutation has on fitness and its recessivity (the worst is a mutation, the higher is its recessivity).


protected by AliceD Apr 28 '15 at 2:08

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