(Image: Jimmy Turrel)
IT TOOK a rather unremarkable garment for people to begin to question their view of reality. On 26 February this year, a photo of a dress went viral – not for its stylishness, but because of its chameleonic colours. Some saw it as blue and black, while others thought it white and gold. Still others, to their enduring unease, saw first one combination, then the other.
The discussions that rippled across the web as a result illustrated a fundamental truth: colour is one of the most vivid and personal experiences we have. But while colour feels extremely real and present, we are still learning exactly how events in our evolutionary past combined to create our particular form of colour vision – and beyond the odd optical illusion, just how important it has been in making us who we are. “Humans wouldn’t be here if we didn’t have colour vision,” says Jay Neitz of the University of Washington in Seattle.
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The first thing about colour is that it doesn’t exist beyond the beholder. We can’t be sure a goldfinch will appear the same sprightly yellow to anyone or anything that sees it. What does exist, though, is its tendency to absorb almost all the light that shines on it, and to reflect the remainder back into the world.
That reflected light pours into your eye, illuminating its retina – a wall of cells that, under magnification, looks like it is covered by a shag carpet. Some of the strands are cone cells, housing light-sensitive proteins called cone opsins; others are rod cells, which allow us to see in low light.
Seeing in ultraviolet
Most people have three cone opsins, each most sensitive to a different wavelength of light: labelled short, medium and long wavelength or simply blue, green and red. The brain’s visual system compares the messages from all three to assess the wavelength mix striking the eye. The result is something like a three-note chord – a harmony that your brain assembles, with each colour having its own particular qualities. Subtle differences in tonality allow us to distinguish something like a million of these chords, each representing a different shade of colour.
The first opsins appeared more than 600 million years ago, and possess them. In the first instance they acted as a basic light sensor. But as more intricate visual systems emerged – , which first appears in fossils from around 520 million years ago – so opsins, too, have evolved. Creatures have tweaked the versions they inherited, duplicated them, lost them and shifted their sensitivity from one wavelength range to another. Humans may have three opsins, but goldfish have four, dogs two and mantis shrimp 12. The relationship between the opsins of mice and us, say, is not clear-cut. “It’s not a given that ours derived from theirs, or what our last common ancestor had,” says , a molecular biologist at the University of California, Davis.
It does seem that the common ancestor of mammals and fish had four opsins – as many fish, reptiles and birds descended from that common ancestor still do today. These include one that responds to ultraviolet light, meaning they can perceive light that is invisible to us. Since that common ancestor, though, the story of opsin evolution in mammals has been “a history of loss”, says , a vision researcher at Lund University in Sweden.
For a start, some time in the early evolution of mammals half of the opsins fell by the wayside – perhaps because our ancestors became nocturnal and relied more on the use of low-light rods than colour-responsive cones. Then one of the two remaining opsins, possibly the ultraviolet one, underwent a transformation: in effect, it became our blue opsin (see diagram).
Biologist , Georgia, has recently suggested that the only way this could have happened was if the seven necessary alterations in the protein code came in a precise sequence. Why did those changes stick? No one knows for certain, though it could be that a shift to a blue opsin reduced blurriness and improved resolution, says , a neurobiologist who studies colour vision at the University of Cambridge. The move may also have freed our ancestors to cut down the amount of damaging ultraviolet penetrating the eye during daytime activities without compromising their vision, says , Santa Barbara. Whatever the reason, the modified opsin proved useful – so useful that it remains with us today.
One consequence of this evolution is that our blue opsin is still sensitive to some ultraviolet light. Normally, the cornea and lenses of our eyes absorb this light before it reaches the retina. But sometimes when people being treated for cataracts have their natural lenses removed, they begin to see patterns on flowers and appear on objects that used to look black. The French impressionist painter Claude Monet, for instance, had cataract surgery on his left eye at the age of 82, and some have speculated that it accounts for the blue and violet hues of his final paintings.
For dogs, cats, horses and hyenas, the story of vision ends there with two opsins. Even many new-world monkeys, our cousins in the primate family, only have two. Of the mammals, only some old-world monkeys and the great apes – humans included – developed trichromacy, the three-colour system we retain today. That happened between 30 and 45 million years ago, when first the gene for the red opsin duplicated and then mutations shifted the sensitivity of the duplicate into the green wavelengths. With it, we went from being able to distinguish some 10,000 shades to a million.
Why did this new form of colour vision take over? One long-standing theory is that being able to distinguish calorie-rich, reddish fruit from the surrounding green foliage, as this adaptation allowed, would have given our ancestors a distinct advantage. “I still think it’s a very plausible hypothesis,” says Mollon. “Sometimes, tongue in cheek, I have said that humans and the whole primate lineage are an invention of trees for propagating themselves.”
Mutants among us
Mollon thinks that this might have been about more than just fruit. Tender young leaves, other primates and their markings, certain types of predatory snake – “all these would be visible against a variegated background once you could compare the signals from long- and middle-wave pigments”, he says. Neitz goes further. He suggests that by allowing us to ingest more calories, this development allowed us to grow bigger brains, starting a positive spiral that allowed us to use colour vision in ever more sophisticated ways.
Ultimately, it’s the complexity of the way that such big brains construct colour that helps to create illusions such as that of the dress (see “The mystery of ‘The Dress’“). Regardless of trichromacy’s role in that development, it has created other fascinating quirks of human colour vision. The red and green opsin genes reside on the X chromosome, of which women have two and men only one. About 6 in 100 men have mutations in one of these genes that make the red and green opsins very similar. A woman with this mutation has another X chromosome that usually provides a normal opsin, but a man has no back-up, making it more difficult for him to tell reds from greens. He is colour-blind.
We have known about colour blindness since at least the 18th century (see “Eyeballs with secrets“). But with two X chromosomes, women with a mutated red or green opsin can end up with four types of opsin. That means that they might, if their brains can make sense of it, create chords with four notes, enabling them to distinguish some 100 million colours.
The Dutch scientist Hessel de Vries was the first to make passing reference to this, when he that daughters of colour-blind men responded differently to colour vision tests than other people. (Men, of course, get their X chromosomes from their mothers and pass them on to their daughters.)
Decades later, Mollon came across de Vries’s paper. Together with neuroscientist Gabriele Jordan, now at the University of Newcastle, UK, he began to test women with four different opsins. In 2010, the team revealed that they had found one woman, a doctor in Newcastle, who could distinguish shades mixed by a computer that appear identical to everyone else. She is the first of her kind known to science (). Why her, and not other women with four opsins? “That’s a tough one,” says Margaret Livingstone, who studies how the brain processes colour at Harvard Medical School. It might be that some extra change needs to happen in the neural circuitry to make sense of that extra information, or that the extra opsin gene is not expressed in the retinas of everyone who has it.
And it’s not always quite as simple as more opsins, more colours, as evidence gathered from mantis shrimp, with their 12 types of opsin, suggests. Last year, a team led by Justin Marshall at the University of Queensland in Brisbane, Australia, showed that mantis shrimp trained to respond to colours using food rewards stopped being able to distinguish between colours much earlier than humans ().
The explanation for their large number of opsins might lie in their neural processing power. “It might just be an adaptation for not having a big enough brain to be able to do real comparisons of colours,” says Michael Bok at Lund University. Our back-end processing lets us perceive colour as a symphonic experience that can convey meaning and beauty. But for the mantis shrimp, it may be a behavioural trigger: the colour pattern of a predator means time to zip away; that of a potential mate indicates it’s time to stick around.
“It might just be an adaptation for not having a big enough brain”
It’s natural that we should be curious about what creatures with more opsins see. But it seems our meagre three, coupled with our enormous brains, haven’t done so badly for us. It may have taken a dress to alert us to the intricacies of our own colour vision – but certainly, somewhere along the line, it has become about a lot more than spotting fruit.
Eyeballs with secrets
Colour blindness is a condition that mainly affects men. Three-quarters of colour-blind men have the standard three types of retinal colour receptor proteins, known as opsins, one of which is faulty. But about a quarter have lost an opsin altogether, because the gene that codes for it has been lost.
One of the earliest descriptions we have of colour blindness turns out to be a case of a missing opsin. In a 1794 lecture in Manchester, UK, celebrated 18th-century chemist John Dalton noted, “I have often seriously asked a person whether a flower was blue or pink, but was generally considered to be in jest.”
Dalton thought the fluid in his eyes might be tinted, but when (according to Dalton’s wishes) his doctor sliced open his eyeballs after his death, the fluid was clear. The doctor was unable to solve the mystery, but the eyeballs were preserved, and in the 1990s, neuroscientist John Mollon at the University of Cambridge and his team took samples for DNA testing. Dalton, they discovered, had no gene for the green opsin.
They bolstered their DNA evidence by comparing the optical qualities of 18th-century red sealing wax with deep green laurel leaves, which Dalton wrote were exactly the same colour to him. They found that, for someone who is missing the green opsin, the light reflected off those items should make them appear very similar. ().
Hiding in plain sight
The Ishihara test for colour blindness, published in 1917, is still commonly used today. Named after its creator, the Japanese ophthalmologist Shinobu Ishihara, the test employs a series of round images made up of dots. Each image contains numbers and patterns that are only identifiable by hue. In the test on the left, people with normal colour vision should be able to pick out the number five, while people with red-green colour deficiency – who have difficulty distinguishing between green and red – cannot. In the test on the right, people with red-green colour deficiency perceive the digit two, while people with normal vision see no number.
The mystery of “The Dress”
If you found yourself bamboozled by the picture of the blue and black (or was it white and gold?) dress that took the internet by storm earlier this year, you can comfort yourself that at least part of the story is that your brain is so very complex.
The white-gold effect comes about because the brain attributes the brightness of the image to the garment (which, as is clear from the picture above, was sold as blue-black), rather than to the light pouring onto it. This unconscious ability to compensate for an object’s surroundings and the quality of the light is ancient – certainly older than primates – but there’s more to it than that.
Expectation, for instance, plays a role in what we perceive. Some people may have thought the dress was a wedding dress, helping to tip the balance towards white; others may have read that it was blue, pushing things the other way. Jay Neitz of the University of Washington in Seattle sees it as white, but is nevertheless also aware of the blueness coming from the image. For him, the variation in perception illustrates the rare subtlety of the interplay between our eyes and our brains. “I think that that’s a primate thing. That’s a big brain thing,” he says.
This article appeared in print under the headline “Eye of the beholder”
