The Genetics of White and Gold, Blue and Black: A Holler to 23andMe

The internet is currently losing its collective composure over the perception of colour in the following unremarkable photograph:

Blue and black, or white and gold?

Buzzfeed’s explanation invokes the illusion of compensation; that a single shade can be perceived in multiple ways depending on the lighting context (see image below). There is an excellent write up of the illusion on Jerry Coyne’s blog so I won’t go into any more detail on it here. But you should click through to see a vivid example of the illusion in action.

Compensation illusion: A and B are the same shade.

What I am more interested in is the ratio of “Black and Blue”, to “White and Gold” in that Buzzfeed survey. The sample size is large (>200000 people have voted), and those numbers look suspiciously Mendelian, which got me thinking that perhaps there might be an opportunity to look for a genetic link to colour perception.

Source: Buzzfeed

For those who remember high school genetics, Mendel was the Monk who discovered genetic inheritance by crossing pea flowers of varying colours. When we refer to simple inheritance of traits they are often described as “Mendelian”. At a single locus, perhaps there is a dominant ‘White and Gold’ gene, and a recessive ‘Blue and Black’ gene. At equal frequency in the population, one would expect the phenotypes (white/gold versus blue/black) exactly as shown in the survey. That’s a lot of “ifs”, and highly unlikely, but it is possible that there may be some genetic control underlying this variation in perception.

Mendelian inheritance

Is it possible that compensating in colour perception could be partly influenced by just one locus? It sounds absurd, but if this is not some elaborate trolling then it might actually be a real possibility.

This is where you come in 23andme! As holder of one of the greatest collections of human genetic variation data, I implore you to carry out the white and gold, blue and black survey yourselves. Linked to 600,000 single nucleotide polymorphisms for over 1 million people, we could get a pretty powerful association study done really quickly. The result could tell us something fascinating about the genetics of perception.

Die Selfish Gene, Die.

I was recently asked by a friend for my opinion on David Dobbs’ piece “Die Selfish Gene, Die.” The article spins a yarn on why Richard Dawkins’ “Selfish Gene” thesis is sunk and the battle for updating it with a new theory of “genetic accommodation”.

It has attracted much attention as a great piece of science writing popularising the battle for a paradigm shift in genetics and evolution. Unfortunately its inaccurate and a bit too puffed up on its own bravado. My brief statement is below, however Jerry Coyne, Richard Dawkins and PZ Myers provide a more thorough commentary.


Dobbs’ article describes a battle of two straw men. 

The term “genetic accommodation” is a new one to me, but the description of it sounds like phenotypic plasticity together with pleiotropy and epigenetics in a fancy jacket, but maybe we needed a word for that. Nonetheless, contrasting it with the selfish gene hypothesis is a false dichotomy. The messy truth for many traits lies somewhere in between, where the convoluted cascade of genetic-epigenetic-genetic interactions involved in “expression” will face selection as soon as its resultant phenotype hits the environment. 

The complexity of gene expression via interactions between genes and epigenetics (non-DNA inheritance) is blowing a lot of our heads off right now. It’s chaotically complex in there. I think the article therefore makes a mistake in referring to “gene expression” as a singular process.

Work I saw presented by John Mattick from the Garvan Institute provides a good example. Gene expression in human neurons can be governed by the interaction of RNAs, binding to “non-coding” DNA and interacting in 3 dimensions with complex protein molecules. In other words, it starts with a gene, which makes an RNA. That RNA’s action depends on the interaction between its sequence and where it binds on the genome. The sequence of DNA to which it binds, governs how it binds; simple like a zip, or more complex and looped up. Along comes a protein molecule (encoded earlier, elsewhere, by another gene) and the molecular properties of that gargantuan tangle of amino acids determine how it interacts with that looped up bit of RNA stuck to the DNA. This binding provides but a step in some long chain of protein interactions in a biological pathway. 

This kind of combinatorial complexity of interactions provides huge plasticity of action for a single set of tools (the genome).

One could argue that the first step of environmental interaction of any gene is the “environment” of the genome and epigenome it inhabits. This could still be squared with the selfish gene thesis.