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Duly Knotted: A Problem for Evolution


Bacteria, yeast and humans have very similar proteins that form slipknots. As Ann Gauger has already noted here, this would seem to pose a knotty problem for evolution. Evolutionary theory, however, is like The Blob. It sweeps up every obstacle in its path and moves on, growing bigger, fatter and uglier all the time.

Evolution's immunity from falsification is evident in a Science Daily article, "Untangling Knots, Slipknots in Species Separated by a Billion Years of Evolution." So you think a string of amino acids that can automatically fold itself into a slipknot gives some pretty good evidence of intelligent design? The suspicion might seem more like a sound inference when you realize that this slipknot performs a vital function: slipknot proteins, that "might look like shoelaces for cells," actually "stick through the cell membrane like pins in a pin cushion and help the cell sense and respond to its environment." That inference might be considered confirmed by the knowledge that evolutionists admit the basic design of slipknot proteins has not changed for a billion years, and is basically the same in bacteria and humans.

Ah, but evolutionists are clever. Since all they have to do is assume their belief to be true and then go on from there, the rest is easy: make up a story to fit the observation into the grand evolutionary tale. A good short story, however, requires a source of conflict. Joanna Sulkowska, from UC San Diego, shows how this is done for "strongly conserved" proteins:

"The slipknot is surprisingly conserved across many different families, from different species: bacteria, yeast and even human," Sulkowska said. "They have really different evolutionary pathways, yet they conserve the same kind of motif. We think the slipknot stabilizes the location of the protein inside the membrane."
Lest the National Center for Science Education fire up the red alarms over a potential ID flare-up, Sulkowska's story quickly calls on Evolution to douse the flames with Darwin magic water:
Although a typical protein folds in a fraction of a second, researchers can see from simulations that knotted and slipknotted proteins would take longer to reach their folded structures than would unknotted proteins. Sulkowska said the extra effort to fold into knotted shapes must have a biological payoff or nature would have selected an easier path....

"Evolution didn't redact these proteins," she said. "They still fold, so they must have some function."

That's why they are strongly conserved, don't you see? Evolution, the Great Arbitrator, found the amino acid sequence for slipknots functional, so he/she/it didn't "redact" them. In evolutionary short stories, Evolution is always the hero/heroine/all purpose Theory Rescuer. Even as sponges were turning into dinosaurs and yeast evolved into Neanderthals, these slipknot proteins (and the genes that code for them) were destined for a dead-end job, the same-ol' same-ol' for a billion years.

Now take the Darwin-tinted glasses off and look at these things again. Could you design a chain that folds into a slipknot? That's pretty amazing as a magic trick, but these knots actually do something: they stabilize the location of proteins in cell membranes, just like a rancher might tie a well-designed knot to stabilize a rope in a fencepost. The active sites of these proteins are often deeply embedded in the fold. How did "Evolution" do that? Where's the payoff?

Finding the payoff is no easy task, but there are genomic clues. For instance, she said researchers suspect that "active sites" that control the folding pattern for knotted proteins often wind up inside the knotted structures after folding is complete. It's possible, she said, that knotted proteins also have chaperone proteins that help the process along. Another mystery to be solved is how the body degrades knotted proteins; breaking down misfolded proteins is a normal function for healthy cells, and breakdowns in this process have been implicated in diseases like Alzheimer's and Parkinsons.
It sounds like the problem just got knottier. Now evolutionists have to account for those chaperones, too. They have to explain why an unguided process that produces disease when it fails succeeded in generating complex, functional structures.

Sulkowska admits that "we already know from experience how useful knots are." That's why the inference to intelligent design, like Stephen Meyer explains, is not based on what we don't know, but rather on what we do know from uniform experience -- in other words, not what we know not, but what we know about knots. They're functional. They're intelligently designed.

By contrast, the knots that occur by undirected processes, like those aggravating tangles in fishline, usually take intelligent design to untangle. That happens in life, too. Intelligently designed knots are good, but tangled ones lead to disease. Knots are "almost everywhere," Sulkowska understands: "in your shoes, in moving cargo, in physics as part of string theory. Now we hope to make this knowledge useful, maybe as a way to design new types of very stable proteins for disease treatment." OK, so what's evolution got to do with it?

Watching an evolutionist try to explain a conserved functional protein is like watching a magician say "Abracadabra" while doing a rope trick. We know from uniform experience that ropes don't really act that way without intelligent design. Entertaining as the act may be, you know there's sleight-of-hand, misdirection and storytelling going on.

Photo credit: Whatknot/Flickr.