Morton's Toe: Dominant or Recessive?
Morton’s Toe: Dominant or Recessive Trait?
My second toe is longer than my first toe. As a young child, I thought that this was the norm, but gradually became aware that for a great number of people the second toe is of equal length or shorter than the first toe. I set out to do some research to find out why I had the freaky long second toe – also known as Celtic toe, or, more commonly, Morton’s toe.
The research began with learning that Morton’s toe is hereditary. Furthermore, it appears to be a dominant trait, according to McKusick.
Kaplan (1964) claimed that the relative length of the hallux (footnote) and second toe is simply inherited, long hallux being recessive. In Cleveland Caucasoids the frequency of the dominant and recessive phenotypes was 24% and 76%, respectively. Usually the first toe is longest, although in the Ainu the second toe is said to be longest in 90% of persons. In Sweden, Romanus (1949) found the second toe longest in 2.95% of 8,141 men. Romanus thought that the long second toe is dominant with reduced penetrance. Beers and Clark (1942) described a family in which long second toe occurred in 10 persons in 3 generations (McKusick, 1998).
Although the Mckusick information was quite convincing, additional information was needed to provide further support to the claim that Morton’s toe is, indeed, a dominant trait. The results of that accumulative research actually supported nothing, as Morton’s toe is said to be both dominant and recessive, depending on the source. One reason for there being no definitive answer is that Morton’s toe, like several other traits, was previously believed to be Mendelian, but it is now believed to be based on more complex genetic models. Therefore, there appears to be conflicting believe as to whether this phenomenon is the result of a dominant or recessive gene trait. Hence the representation of Morton’s toe as a dominant trait in this essay is simply arbitrary.
Punnett square is a chart used by geneticists to show all possible allelic combinations of gametes in a cross of parents with known genotypes. Predicted offspring genotype frequencies can be calculated by tallying the allelic combinations in the P-square. As neither of my children shares this trait, I will use a Punnet Square to illustrate how they seem to have inherited their father’s toes, or more accurately, not mine. For the purpose of this demonstration, Morton’s toe is assumed to be a dominant trait.
This Punnet Square represents Parental Genotype Mm X Parental Genotype mm
m Mm mm
m Mm mm
The resulting genotype frequencies are:
mm: 2 (50.0%)
Mm: 2 (50.0%)
All four possibilities for offspring will not have Morton’s toe, but will carry the gene for it. There were actually two offspring, neither of whom have Morton’s toe. But since they carry a recessive gene for it, one of the offspring was able pass it along to one of her own offspring.
Punnett Squares can be used to calculate the probability of any genetic trait appearing in offspring, including these traits as shown in the Dominant and Recessive Traits handout web page (http://www.blinn.edu/socialscience/ldthomas/feldman/handouts/0203hand.htm).
Dominant Traits Recessive Traits
Brown eyes Grey, green, hazel, blue eyes
Dimples No dimples
earlobes Attached earlobes
Freckles No freckles
lips Thin lips
Farsightedness Normal vision
vision Color blindness
Of course, this is just a small representation of the endless possibilities of traits one might inherit, but it’s enough to give a basic idea of how the principle works. Note that in the table above, the farsightedness trait is dominant over the recessive trait for normal vision, while normal vision is dominant over nearsightedness and color blindness, indicating that a trait might be either dominant or recessive, depending on what it’s being compared to.
Finally, I would like to conclude by stating that although Mendalin was able to found modern basic genetics involving single gene traits, recent studies have found a number of variables that are not explained by Mendelian laws. For instance, some complex traits are determined by multiple genes and environmental factors, and therefore do not conform to simple Mendelian patterns. Such complex non-Mendelian disorders include heart disease, cancer, diabetes, and more. Fortunately, these disorders are becoming more experimentally accessible with recent advances in genomics. Once again, science will prevail.