The Case for a Creator - Lee Strobel [109]
Behe didn’t look impressed. “A motor protein that has been transporting cargo along a cellular highway might not have the strength necessary to push two microtubules relative to each other,” he replied. “A nexin linker would have to be exactly the right size before it was useful at all. Creating the cilium inside the cell would be counterproductive; it would need to extend from the cell. The necessary components would have to come together at the right place at the right time, even assuming they were all pre-existing in the cell.”
“Isn’t it possible that they might all come together by chance?” I asked.
“It’s extraordinarily improbable,” he replied. “Let me illustrate it for you. Say there are ten thousand proteins in a cell. Now, imagine you live in a town of ten thousand people, and everyone goes to the county fair at the same time. Just for fun, everyone is wearing blindfolds and is not allowed to speak. There are two other people named Lee, and your job is to link hands with them. What are the odds that you could go grab two people at random and create a link of Lees? Pretty slim. In fact, it gets worse. In the cell, the mutation rate is extremely low. In our analogy, that would mean you could only change partners at the county fair one time a year.
“So you link with two other people—sorry, they’re not the other Lees. Next year, you link with two other people. Sorry, no Lees again. How long would it take you to link with the other Lees? A very, very long time—and the same is true in the cell. It would take an enormous amount of time—a prohibitive amount of time—even to get three proteins together.
“To make it even more difficult, a recent study in Science magazine found that half the proteins in a simple yeast cell don’t function alone, but they function as complexes of half a dozen proteins or more. Up to fifty proteins are stuck together like cogs in a machine. Of the other fifty percent, most are in complexes of three or four. Very few work as single, Lone Ranger proteins. So this is a huge problem not only in cilia but in other cells too.”
“Some scientists have pointed out that there are examples of other cilia that don’t have some of the parts that you contend are essential,” I said. “One said, ‘In nature, we can find scores of cilia lacking one or more of the components supposedly essential to the function of the apparatus.’ Doesn’t the existence of simpler cilia refute your contention that they are irreducibly complex?”
“If you could point to a series of less complex structures that progress from one to the other in order to create the cilia I’ve described, then, yes, that would refute me. But that isn’t the case,” he said. “What the critics say is that you can take away one of the several microtubules and the cilium would still function. That’s fine. You still need all the basic components—microtubules, nexin, and dynein.
“Let me give you an analogy. Some big mousetraps—actually, they’re rat traps—have double springs to make them stronger. You can take one spring away and it would still work to a degree. In a sense, the second spring is a redundant component. The cilium is the same way; it’s got some redundant components. You can take one of the microtubules away and it will still function, though maybe not as well.
“But evolution does not start with the completed trap or completed cilium and take parts away; it has to build things up from the bottom. And all cilia have the three critical components that I’ve mentioned. There have been experiments where scientists have removed one of the three and the cilium doesn’t work. It’s broken—just like you’d expect it to be, since it’s an irreducibly complex machine.”
THE WORLD’S MOST EFFICIENT MOTOR
As amazing as the cilium is, I was even more fascinated by another biological machine for propelling cells