If, like many a disappointed Muggle, you were devastated when your Hogwarts acceptance letter did not arrive on your 11th birthday, you can rest safe knowing that you only have your parents to blame. The wizarding gene is almost certainly a non-Mendelian, dominant and autosomal gene.
J.K. Rowling has stated that the wizarding gene is dominant, leading to many angry Muggles arguing that this doesn’t explain the existence of Muggle-born witches and wizards, Squibs (non-magical children born to magical parents), nor the occasional resurgence of the wizarding gene in the descendents of Squibs. This would be a sound argument if the wizarding gene followed the Mendelian pattern of inheritance.
If you studied biology in high school, you might remember Gregor Mendel, the Silesian scientist, friar and Muggle who, after his death in 1884, was recognised as the founder of genetics. Mendel focused on plants, studying over 29,000 pea plants and looking at the frequency of different characteristics such as flower colour, seed shape and plant height. Without having any knowledge at all of chromosomes and DNA (discoveries that would come much later), Mendel was able to draw generalisations from what he found and described two laws: the Law of Segregation describes how each individual has two alleles – or versions of each gene – one from each parent, and each parent passes one of these alleles at random on to their offspring. Which allele is expressed depends on ‘dominance’, which may be complete (for example, the allele for brown eyes is dominant, so an individual with one brown eyed allele and one blue eyed allele would have brown eyes), incomplete (for example, alleles for snapdragon flower colours are either red or white – if a plant has one of each allele, it will be pink), or display co-dominance, where both alleles are expressed at the same time (blood types, for example – if an individual has inherited both the A and B blood type allele, their blood type will be AB).
Mendel’s second law, the Law of Independent Assortment, describes how genes are passed on from parent to offspring independently of each other – that is, the random selection of one allele for one gene has nothing to do with the selection of another. For instance, there is no relation between whether or not a person has freckles, and is double jointed.
Like many brilliant discoveries, Mendel’s work was reviled at first, and only recognised for its genius (and truth) years later. But Mendel’s laws (termed Mendelian inheritance) do not describe the inheritance of every gene. Some genes are linked (for example, blonde hair/fair skin, and dark hair/dark skin), some traits are controlled by multiple genes (like arthritis), and some traits are caused by ‘trinucleotide repeats’, like Huntington’s disease (more on that later). These forms of inheritance are called non-Mendelian.
In a well-referenced, six-page epic scientific paper published in the popular science journal, Tumblr, Andrea Klenotiz of the University of Delaware outlines how “magical ability could be explained by a single autosomal dominant gene if it is caused by an expansion of trinucleotide repeats with non-Mendelian ratios of inheritance”.
DNA is made up of sequences of four nucleotide bases – guanine, cytosine, adenine and thymine. The order of the bases determines what products are made (that is, what the gene does). Trinucleotide repeats – repeats of a sequence of three nucleotides – are a sequence that can result in non-Mendelian genetic disorders. An example of this kind of inheritance is Huntington’s disease, which is caused by cytosine-adenine-guanine (CAG) repeats. Klenotiz magically transfigures this model to apply to the wizarding gene, which, like the Huntington gene, is dominant and autosomal (that is, not linked to sex chromosomes). In case of Huntington’s, a ‘normal’ person has about 11-34 CAG repeats in the gene of interest, but when a person has more repeats – about 42 to over 66 – an abnormal protein is transcribed, causing serious symptoms.
These sequences are often unstable, and the trinucleotide repeat sequences can become longer over the generations through mutations called genetic expansion. Klenotiz explains that if, for example, the threshold for magical ability were 100 repeats, two Muggles with 90 repeats each could therefore produce a magical child. Given that this event would be more likely in Muggle parents with higher (but still ‘normal’) numbers of repeats, such a couple would be more likely to have multiple magical children, perhaps explaining the Creevey brothers. Such instances would be rare, but certainly possible.
The idea of genetic expansion could also explain the wide variation in the strength of magical powers. In the case of Huntington’s, individuals with higher numbers of CAG repeats tend to display an earlier onset and more severe symptoms. It follows, then, that a greater number of repeats may result in a more powerful magical ability, perhaps giving a genetic reason for why some wizarding families seem to be more powerful than others.
As for Squibs, whilst rare, it is possible for some trinucleotide repeats to be deleted during transcription. This could result in a non-magical child with a number of trinucleotide repeats just under the threshold for magical ability. Whilst Squibs have no magical ability, they are still likely to have a higher than average number of repeats, perhaps explaining the occasional resurgence of magical ability in the offspring of Squibs (though it is important to note that a Squib with 90 repeats would be no more likely to produce a magical child than a Muggle with 90 repeats).
Klenotiz’s model goes further than any other so far in explaining the inheritance of the wizarding gene. But different types of inheritance – and the role of environmental factors – are being discovered all the time. So if any budding geneticists out there are taking a break from studying for their N.E.W.T.s and are able to come up with their own model, send me an owl and we can discuss it over butterbeer and chocolate frogs.
You can read Andrea Klenotiz’s full dissertation at http://ow.ly/o74pl