Arendt's discovery leads to yet another question. It is one thing for eyes to share common parts, but how can eyes that look so different—such as those of worms, flies, and mice—be closely related? For the answer, let us consider the genetic recipe that builds eyes.

At the turn of the twentieth century, Mildred Hoge was recording mutations in fruit flies when she found a fly that had no eyes whatsoever. This mutant was not an isolated case, and Hoge discovered that she could breed a whole line of such flies, which she named eyeless. Later, a similar mutation was discovered in mice. Some individuals had small eyes; others lacked whole portions of the head and face, including their eyes. A similar condition in humans is known as aniridia; affected individuals are missing large pieces of their eyes. In these very different creatures—flies, mice, and humans—geneticists were finding similar kinds of mutants.

A breakthrough came in the early 1990s, when laboratories applied new molecular techniques to understand how eyeless mutants affected eye development. Mapping the genes, they were able to localize the bits of DNA responsible for the mutations. When the DNA was sequenced, it turned out that the fly, mouse, and human genes responsible for eyelessness had similar DNA structures and sequences. In a very real sense, they are the same gene.

What did we learn from this? Scientists had identified a single gene that, when mutated, produced creatures with small eyes or no eyes at all. This meant that the normal version of the gene was a major trigger for the formation of eyes. Now came the chance to do experiments to ask a whole other kind of question. What happens when we mess with the gene, turning it on and off in the wrong places?

Flies were an ideal subject for this work. During the 1980s, a number of very powerful genetic tools were developed through work on flies. If you knew a gene, or a DNA sequence, you could make a fly lacking the gene or, the reverse, a fly with the gene active in the wrong places.

Using these tools, Walter Gehring started playing around with the eyeless gene. Gehring's team was able to make the eyeless DNA active pretty much anywhere they wanted: in the antenna, on the legs, on the wings. When his team did this, they found something stunning. If they turned on the eyeless gene in the antenna, an eye grew there. If they turned on the eyeless gene on a body segment, an eye developed there. Everywhere they turned on the gene, they would get a new eye. To top it all off, some of the misplaced eyes showed a nascent ability to respond to light. Gehring had uncovered a major trigger in the formation of eyes.

Gehring didn't stop there; he began swapping genes between species. They took the mouse equivalent of eyeless, Pax 6, and turned it on in a fly. The mouse gene produced a new eye. And not just any eye—a fly eye. Gehring's lab found they could use the mouse gene to trigger the formation of an extra fly eye anywhere: on the back, on a wing, near the mouth. What Gehring had found was a master switch for eye development that was virtually the same in a mouse and a fly. This gene, Pax 6, initiated a complex chain reaction of gene activity that ultimately led to a new fly eye.

We now know that eyeless, or Pax 6, controls development in everything that has eyes. The eyes may look different—some with a lens, some without; some compound, some simple—but the genetic switches that make them are the same.

When you look into eyes, forget about romance, creation, and the windows into the soul. With their molecules, genes, and tissues derived from microbes, jellyfish, worms, and flies, you see an entire menagerie.

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