Page 44: Fruit Flies

Evolution speeds vary a lot.

Elephants come to sexual maturity late, have a very long gestation period, and generally stay within a tight social framework. The opportunity for new genes to be introduced to the pool is limited by social bonds and relatively infrequent reproduction holds down the number of mutations. In other words, Elephants will tend to evolve slowly.

On the other extreme, consider the fruit fly. The female fruit fly reaches sexual maturity in 8-12 hours. About 7 days later, she will produce a new generation. Not only that, she will mate with multiple males, producing a sort-of "proportional representation" set of offspring of mixed genetic material. There's a lot of mixing and there are a lot of babies. That means there are lots of new genetic combinations and lots of mutations. In other words, fruit flies evolve very quickly. This makes them useful.

Scientists like three things about the fruit fly. First, their genes are relatively simple and easy to manipulate; second, they produce new generations very quickly; and, third, there aren't a lot of activists marching around with signs that read "save the fruit fly".

I got the fruit fly example from Matt Ridley's great book The Agile Gene, in which he talks about the fruit fly several times. The story he tells in the chapter Learning Lessons (page 180 of the paperback) is fascinating.

Did you know fruit flies can learn? Scientists at CalTech figured this out by spraying a smelly chemical at a box full of fruit flies right before electrifying a metal plate on which the flies were sitting. This may sound cruel, but, hey, they are only fruit flies (see what I mean about the activists?). The scientists found out that some of the fruit flies were able to learn that when they smelled the bad smell they better get flying or else get shocked.

But not all the fruit flies learned. The scientists observed that a fruit fly had to have specific genes (17 of them) in order to remember the link between the stink and the shock. The genes make it possible for the fruit flies to learn, but they don't contain any information. The learning comes from the shocking. Both the genes and the experience are necessary. The shocking experience causes certain neurons to weld together (using a protein made possible by the genes) in a specific part of the fruit fly's brain. It is the whole system of genes-proteins-neurons-brain that enables the fruit fly to recall that the stink and the shock are linked. The system "hard-wires" the memory into the fly's brain.

The breeding characteristics of the fruit fly made this scientific discovery possible. Because of the fast fruit fly lifecycle, it was possible to breed a few flies, see which ones can learn, separate them, then breed them again. After a few generations (a couple of weeks), you have "pure" learners and pure, well, dunces. It's really cool. It's what nature does, only on fast-forward.

Meanwhile, in a separate experiment, some other scientists had inserted a mutant gene in some flies. Believe it or not, this mutation made it so that a particular fly would be paralyzed in hot weather. Literally, at 20 degrees C the fly is perfectly fine, at 30 degrees C, it drops from the sky. Amazing.

Then they combined the two experiments. The scientists switched the heat-sensitive paralyzing gene from the part of the brain that controls motion to the part of the brain that controls memory. So now their flies could fly in hot weather, but couldn't use the memory parts of their brains that had been hard-wired with the stink-shock memory. Sure enough, in cool weather the flies remembered the implications of a bad smell and in hot weather they got shocked. Astounding.

So, basically, they used fruit flies to prove that memories get permanently or temporarily "hard wired" in our heads by specific proteins generated by specific genes. And it was all made possible by our friend the frisky, fast-evolving fruit fly.

Page 20: CCR-5 Receptor Mutation

Without doubt, my favorite things to write in Old Blood were the genetic discussions. I just love them. I wish I could write books on it, like Matt Ridley. His book, Genome, is a perspective changer.

The CCR-5 mutation is an incredibly cool thing that didn't really get a lot of space in the book. So here is a more straightforward telling of the tale:

The way to think about the mutation is this: If you thoroughly spray a nest of, say, 1000 cockroaches with a particular poison and 3 or 4 survive the treatment, what you have neatly done is find the 3 or 4 cockroaches that are immune to the poison. Bingo, you've committed evolution! You have, in a moment of poisonous spray, selected for a particular genetic trait. If the 3 or 4 cockroaches go on to make some baby cockroaches, most or all of their offspring will also be immune to the poison because they inherit the immunity gene from their parents.

The beautifully ironic thing about our 3 or 4 cockroaches is that their immunity gene was probably a reproductive mistake, a flaw, or, more colorfully, a mutation. A mutation that saved their lives.

On a much larger scale, the waves of disease that have washed through the human population, including the black death, cholera, and small pox have acted just like the roach poison above. They, by and large, killed almost everybody that wasn't at least partially immune. Because there wasn't advanced medical care back then, the diseases made a fairly "clean sweep" of the non-immune.

The immunity in humans was likely conferred by a mutation in a receptor, sort of like a door, through which infections sneak into cells. In other words, a few people had a flaw, a mutation, in their CCR-5 receptor. Their flaw was their savior. Correction, the mutation was OUR savior, because if you are of European descent you likely share the mutation. Most of us are mutants.

And we are lucky, for it was not a skill that enabled our ancestors to survive, but rather a lucky genetic break. But isn't all talent some form of genetic lucky break? A big question for human society is whether something that is subject to inheritance and probability is a legitimate differentiator. We tend to be okay with hard work: If hard work made you wealthy you get a smattering of applause. On the other hand, we tend to dislike luck and absolutely loathe inheritance. Many argue that because wealth is often tied to inheritance or luck rather than skill or hard work that confiscatory taxation is justified. Or consider another example, does the inherited hardiness of your genetic stock entitle you to a lifetime of reduced medical costs, or should you pay your "fair share" despite your "innate talent" for surviving disease? What about intelligence? When we all have to get on a spaceship to escape the asteroid, does being "lucky" enough to be smart guarantee you a spot on board? After all, to be smart is to have, at least in part, inherited good genes. These are difficult questions.

Equally difficult is the question of biodiversity. What if our 3 or 4 surviving cockroaches are highly allergic to, something they haven't yet encountered, say, pine nuts? What if being allergic to pine nuts was somehow related to their ability to survive the poison? The lucky survivors would carry a valuable immunity but also a fatal flaw that might not allow them to survive their first contact with pine nuts.  Their luck with poison could be placing them a moment away from extinction.

To wit, what if all the professor-types we shoot into space are too weak to move the big rocks on Planet X. Oops, we should have sent some other folks, too. It's hard to know in advance what will aid survival. Genetic selection is HIGHLY subject to the laws of unintended consequences. [This will form a big part of Bad Blood, on which I am working now.]

Some scientists believe the modern phenomenon of allergies (which have demonstrably gotten more intense over the centuries) is related to diseases such as cholera. The survivors of cholera had an incredibly sensitive, some might say jumpy, immune system that reacted quickly to fight the disease. Those hyper immune systems now go off like alarm bells at the first sign of invasion by, well, pollen. So what was once a BIG blessing is now a minor curse. But it is still working for us, even if we are all sniffly.

Speaking of working for us, it is also thought that CCR-5 mutation is offering at least partial protection against HIV, which may explain why the disease has been more prevalent in Africa and Asia than in Europe or the United States. Another lucky break.

So being lucky is good, luck got us here alive. And now? Embrace your flaws, they may save your life someday.