John Coley at Northeastern University wants to help his biology students “avoid misconceptions about science.” It’s wrong to state, “Zebras developed stripes to avoid predators,” he explains at PhysOrg.
[E]volution doesn’t involve “forward thinking,” or intention — ancestral zebras didn’t sprout stripes to blend in with their surroundings. Rather, given a population of zebra-like animals varying in stripedness, those with abundant verticals had a selective advantage over their plainer relatives: Hence, they were more successful at reproducing, and over time, the stripes prevailed. [Emphasis added.]
Whether this after-the-fact story does any better in explaining zebras is an interesting question. Why should we accept that stripes emerged as a “given”? If stripes provide a selective advantage, why aren’t all prey animals striped, for example horses and cows? Besides, not all zebra stripes are vertical. It’s doubtful that Coley’s story is any less a “misconception” than the alternative he warns against.
But what if biologists were to find a multi-step process that exhibits “forward thinking”? Can evolution account for that? And what if a process shows backward thinking — the ability to recognize that a problem has occurred, and fix it? Let’s examine some cases in the living cell and consider the implications.
Forward Thinking: Checkpoints
Cell division is a carefully choreographed process. Huge amounts of genetic information have to be duplicated with high fidelity. Organelles have to divide and move. Chromosomes have to form and align on a structure called the mitotic spindle. The nuclear membrane has to break down on cue. Molecular “lassos” have to pull the chromosomes apart. After they separate, a molecular cinch has to form on the right axis and tighten, dividing the single cell into two identical copies. It’s a marvel to watch under a microscope.
To ensure fidelity, the cell has a number of “checkpoints” during mitosis. These are go or no-go decision points, where signals give the green light to proceed, or yell “Stop!” if a problem has occurred, or if required elements are not in place. If severe enough, a no-go decision can trigger programmed cell death (apoptosis).
One example of checkpoints is described in news from Johns Hopkins. The title of the article is instructive: “Cellular Sentinel Prevents Cell Division When the Right Machinery Is Not in Place: Machinery Helps Guide Chromosomes During Division.” A research team examined one particular checkpoint mechanism: a protein that counts centrioles.
For cell division to be successful, pairs of chromosomes have to line up just right before being swept into their new cells, like the opening of a theater curtain. They accomplish this feat in part thanks to structures called centrioles that provide an anchor for the curtain’s ropes. Researchers at Johns Hopkins recently learned that most cells will not divide without centrioles, and they found out why: A protein called p53, already known to prevent cell division for other reasons, also monitors centriole numbers to prevent potentially disastrous cell divisions.
Mutations to p53, in fact, are implicated in cancer — a situation where the checkpoint mechanism is broken, leading to uncontrolled cell division. This protein almost seems sentient in its ability to monitor multiple situations:
“P53 was already known to monitor many things, like DNA damage and having the wrong number of chromosomes, that make division dangerous for cells,” says Andrew Holland, Ph.D., an assistant professor of molecular biology and genetics at the Johns Hopkins University School of Medicine. “We’ve discovered one more item on its checklist: centriole number.”
Here’s another example explained from the University of Basel: “Two are better than one — another checkpoint enzyme for flawless cell division.”
Each day, the cells of the human body divide billions of times; this also requires duplication of their genetic information. Errors in cell division can cause tumor formation, and an exact segregation of the DNA (chromosomes) is therefore essential to ensure the health of the whole organism. Prof. Erich Nigg’s research group at the Biozentrum, University of Basel, has demonstrated that the enzyme Plk1 plays a significant role in monitoring the segregation of chromosomes.
Plk1 has checkpoint function
The segregation of the 23 chromosome pairs of human cells only occurs when all parameters are correct. This is ensured by a surveillance process, a so-called checkpoint. Central to this checkpoint is an inhibitor formed on the chromosomes, called mitotic checkpoint complex (MCC), which prevents cell division until all settings on the mitotic spindle, the chromosome segregation apparatus, are correct. “Just like the enzyme Mps1, Plk1 also ensures the assembly of the MCC and finally the inhibition of cell division,” says the first author Conrad von Schubert. “Plk1 thus also has a checkpoint function and consequently safeguards chromosome segregation.”
These are just two illustrations of many safeguards in the cell. If you think about human monitors, like traffic cops or inspectors, they are aware of the downstream consequences of failure to meet requirements. Robots and machines can also be programmed to detect contraband or errors. The robot may be “dumb,” but whoever programmed it had to know; he or she had to have “forward thinking” and plan for the errors or failures to meet requirements.
Backward Thinking: Error Correction
Error-correction strategies exhibit backward monitoring: the ability to detect that a failure has occurred and take appropriate action. This assumes the ability to see what should have happened, and to understand the consequences of letting the failure go uncorrected.
There are numerous repair mechanisms in the cell. One was recently described in news from Lomonosov Moscow State University, “Novel DNA repair mechanism brings new horizons.” Notice the design words in the first sentence. “The DNA molecule is chemically unstable giving rise to DNA lesions of different nature,” the article begins. “That is why DNA damage detection, signaling and repair, collectively known as the DNA damage response, are needed.” The article shows that this is another irreducibly complex program:
During the transcription of information (its rewriting into RNA) the RNA polymerase enzyme “rides” on the DNA chain, and stops when it finds the break. Like a proofreader of a text, RNA polymerase after it is stalled, triggers a cascade of reactions, resulting in the repair enzymes fixing the damaged area. At the same time, the RNA polymerase cannot detect discontinuities present in the other DNA strand.
The scientists found that the machinery can, in fact, proofread the opposite strand from where the break occurred. In their broken English, the Russian scientists could hardly avoid anthropomorphic language:
It turned out that only in nucleosomes, rather than in the histone-free DNA, the enzyme stopped, when the break was present in the other DNA strand. Wherein it did not stop before the break, but immediately after it. It was difficult enough to understand the mechanism that allows it to notice the damage at the “back” of RNA polymerase, as if it had “eyes on the back of the head”, although, obviously, it does not have neither one nor the other.
They went on to find a mechanistic explanation for the processes. But did they find an evolutionary mechanistic explanation? Only in terms of the lack of evolution (e.g., purifying selection):
The highly conserved histones play an important role in this process as changes in their structure are rejected by natural selection. Moreover, the high level of protein conservation just assumes its active participation in many processes.
This is just one of many processes in the DNA damage response repertoire. Damage response is a backward strategy for robustness, as we know by analogy from fire departments, medicine, and error-correcting algorithms in software. Entities don’t have to be sentient to exhibit this kind of strategic behavior; it can be programmed.
“Just in Case” Thinking: Spare Parts
Here’s an item from the American Chemical Society that simultaneously demonstrates design and debunks the myth of “junk DNA” —
Carrying around a spare tire is a good thing — you never know when you’ll get a flat. Turns out we’re all carrying around “spare tires” in our genomes, too. Today, in ACS Central Science, researchers report that an extra set of guanines (or “G”s) in our DNA may function just like a “spare” to help prevent many cancers from developing.
It was thought that “G quadruplexes” were “genetic insults” needing repair. The cell is smarter than they thought:
The researchers scanned the sequences of known human oncogenes associated with cancer, and found that many contain the four G-stretches necessary for quadruplex formation and a fifth G-stretch one or more bases downstream. The team showed that these extra Gs could act like a “spare tire,” getting swapped in as needed to allow damage removal by the typical repair machinery. When they exposed these quadruplex-forming sequences to oxidative stress in vitro, a series of different tests indicated that the extra Gs allowed the damages to fold out from the quadruplex structure, and become accessible to the repair enzymes. They further point out that G-quadruplexes are highly conserved in many genomes, indicating that this could be a factory-installed safety feature across many forms of life.
We can ask, if a manufacturer decides to include a spare tire with a car, what are they thinking? The driver may go for years without a flat. The driver may never need the spare. The manufacturer is looking beyond immediate survival needs. This is “what-if” strategizing. It requires looking both forward and backward: planning ahead for a contingency, and providing equipment and a mechanism for repair if it occurs.
Natural selection cannot do that. It can only respond to the here and now. Once again, too, we see that the mechanism is “highly conserved” across many forms of life. “Factory-installed safety feature” — what a great phrase!
Unthinking: Darwinian Explanations
As we see, living cells employ forward-thinking and backward-thinking strategies. Both strategies require planning outside the immediate situation; they have to “know” the consequences of not meeting requirements or allowing defects to go uncorrected.
Can an evolutionist explain this? Someone like Coley might say, “Given that proteins emerge, the ones that had this ability prevailed.” This ignores the question of how a complex checkpoint mechanism or repair team arose in the first place. It also fails to show how one checkpoint could emerge in a series of checkpoints, any one of which has go or no-go decision-making ability for the cell. Yet without the safeguards, the cell’s lineage would quickly go extinct in a morass of errors. It’s unsatisfying to hear the evolutionist look at complex processes in a cell involving purposeful sequences and responses and dismissively say, “Well, if it didn’t evolve that way, it wouldn’t survive.”
Be it a Rube Goldberg machine or robotic assembly line, any process involving a sequence of events that must occur without error to succeed we know from experience involved planning by a mind. In no case do the parts emerge by unguided processes, because the system cannot work without every part being already in place. For these reasons, we can say that checkpoints and error correction provide not only negative evidence against unguided processes, but positive evidence for intelligent design.