Did you know DNA controls your tan?
Genetic variants influence how much of a tan you are likely to get
When my son turned two, we had the talk – about melanin. He is a child of mixed ethnicities, and was already starting to notice the difference between my South Asian skin and his lighter skin. I chose to give him a scientific explanation, so when repeated, it would in no way be offensive. To this day, he sometimes describes me as “she has melanin”. Yet, try as I might, I couldn’t really predict for him the extent of his tanning ability, until I came across the SLC45A2 gene. A single genetic variant of SLC45A2 is known as the Caucasian tanning allele. It is one of the most significant skin pigmentation predictors. This variant is also known as an ancestry-informative marker (AIM), as it exists in distinctively different frequencies between populations.
Melanin is a natural pigment found in our bodies providing colour for our eyes, hair and skin. Melanocytes, the skin cells that make melanin, can produce two different types of melanin: pheomelanin that is red or yellow in colour and eumelanin, which is brown or black. By default, melanocytes make pheomelanin. However, exposure to ultraviolet (UV) light activates a switch in the melanocytes to start making eumelanin, which is much more efficient than pheomelanin at blocking UV rays.
The need to pigment our skin depends quite a bit on our external environment, since tanning is a natural defence mechanism against UV damage. Darker skin is beneficial if you live in the tropics, where you are constantly exposed to the sun. Pale skin is more favourable if you live in higher latitudes, where sunlight is limited. In low sunlight conditions, pale skin absorbs more UV rays helping to avoid vitamin D deficiency. This explains the many different shades of skin colour we see in people based on their geographical origins.
SLC45A2 encodes a protein is involved in transporting the tyrosine protein that is used to produce melanin. There are two common versions of the SLC42A4 gene that differ at a specific place in the gene (known as the rs16891982 marker). The ancestral form of the gene results in a leucine (Leu) amino acid at this position, while the variant form has a phenylalanine (Phe) amino acid. Amino acids are the individual “building blocks” of our proteins, and changes can affect the function of the resulting protein. In this example, the Phe variant form reduces the activity of the SLC45A2 transporter protein, and is associated with pale skin, as well as lighter hair and eye colour. This Phe variant is highly prevalent in Europeans (e.g. 96% of Germans), but is rarely found in other ethnicities. In fact, over 99% of Asians and Africans have the Leu version of the gene.
When an individual of European descent inherits the Leu version (which happens very rarely), it almost always coincides with black hair. Europeans with the ancestral allele also represent a small group who are able to tan more easily and are at lower risk for sunburn and age spots. However, the Phe variant also has advantages, particularly at higher altitudes (low sunlight, cooler climates), and as a result has been selected for in European populations overtime.
How does this fit into the modern day world where many of us have migrated to climates that are ‘unsuitable’ for our skin? In my case, SLC45A2 could explain the non-appearance of my “dominant” South Asian features in my children. Will my fair-haired, even more pale-skinned daughter be able to tan in the summer like my son or will she burn in the sun? Only time will tell. As we venture onto this new chapter in human evolution, where mixed raced children are slowly becoming the rule rather than the exception, it will be interesting to see the outcome of this real life experiment. Will we eventually re-adapt to match the shade of our skin to our environment? Or will our knowledge of genetics guide our lifestyle choices and be instrumental to an alternate outcome?