In response to my previous post, a comment was made that just because we can imagine a scenario in which an eye could develop step by step through a series of random mutations and natural selection does not exclude it as a possibility. In other words, while Dawkins has snuck sight into his blind watchmaker argument, it does not follow that his theory is wrong. That is a valid point and requires that we take a closer look at the evidence. There are two main areas we can look at to determine whether Paley’s design “watchmaker” or Dawkins’ random mutation and natural selection “blind watchmaker” hypothesis better fit the facts. The first will be at the genetic level where slight changes in DNA are, according to Dawkins, stored. The second is in the organs of sight themselves. The similarities and differences between these organs will be explained based either on common ancestry in the case of the blind watchmaker, or common design in the watchmaker hypothesis.
So let’s begin with the DNA. Our basic understanding is that the subset of DNA known as genes “transcribes” RNA that “translates” into proteins. The proteins then are built together to form and maintain cells, that build organs, that make up the organism. So our watchmakers have to begin their work here. But the evidence at the molecular level is far more complex than our overview of the DNA suggests. It turns out there are many more proteins than there are genes that code for them. This is further complicated by the fact that there are at least three known ways (there may be others ) in which this takes place: “reading” overlapping genes in either the same or opposite reading directions; alternative splicing of RNA where parts of the gene are spliced out or transcribed; and differing initiation reading sites of the same gene1. This allows for the potential of thousands of proteins from a single gene!
The complexity of this system creates enormous challenges for the random mutation/natural selection process popularized by Dawkins because if a single gene makes multiple proteins, mutations of the gene will affect not only the cells and organs you are trying to “evolve” but many others as well. To illustrate this problem consider the challenges faced by Turing and his fellow decoders dramatized in the movie The Imitation Game. They were trying to decode Nazi communications that were encrypted within radio messages. These communications made sense at two levels, the one broadcasted, and the orders encoded within it. It was exceedingly difficult for Turing to discover the orders within the broadcasts because of the degree of sophistication required for the dual messages. Genes are not functioning at two levels of meaning but many levels. The degree to which this is happening is not known, conservative estimates suggest that for humans each gene needs to be transcribed into a minimum of five proteins but there are some examples of genes that produce thousands of proteins. Imagine Turing’s headache if he had to decode between five and a thousand possible codes! We can see genius, order, and sophistication at a deep level in this system, the “watch” we are looking at does not seem to suggest any sort of blindness whatsoever. In contrast, how can random mutations improve the proteins to produce eyes without garbling the multiple other proteins that the gene transcribes for?
When we look at the biochemical expression of the genes responsible for “sight” we see something truly startling. All organisms perceive light using the same basic protein (Here pg 193) Not only that, but all organs for sight are also developed from the same PAX 6 gene!!!. In other words, all eyes in all animals are formed by this master control gene whether they are insects, cephalopods (octopi and squids), or vertebrates like us. It may be tempting to think that this is due to common ancestry but no so-called common ancestor had eyes. In fact, it has long been assumed that eyes evolved independently between 50 and 100 times. Take for example Dawkins use of the squid versus the vertebrate eye. He assumes that the two eyes converged, that is, through a separate history, they came to a similar “superficially convergent” (Blind Watchmaker pg134) looking endpoint. You would not expect then these similarities at the genetic level. But studies have shown that not only are both vertebrate and cephalopod eyes formed by the pax6 master control gene, both undergo the earlier mentioned alternative splicing in the same ways!
The same is true for another example that Dawkins utilizes and that is echolocation in bats. Dawkins highlighted the differences in the way bats echolocate. But it is the differences that are superficial, bats echolocate using the same genes. Not only that, so do dolphins! In fact, it turns out that this is true in all a wide array of genetics. There are master control systems known as hox genes that regulate body types in all animals that serve as three-dimensional blueprints arranging the body plan. They oversee the construction of the animal from head to toe, front to back, and top and bottom. The differences between an insect and a human or any other animal for that matter are found in the expression of these genes rather than the genes themselves. So whether you are talking about heads or toes, mouths or ears, the gut or the sex organs, the same master control genes are involved across the entire swath of animal life.
I am well aware that Dawkins and many other scientists who have a stake in current views of evolution have ways to attempt to explain away the design implications of these findings. But the question is if “apparent” design is evident right down to the genetic level (see as an example one of nine simultaneous gene regulation networks of the fruit fly ) where is there room for a blind watchmaker not to be fatally cut by Occam’s razor?
FROM: Mapping gene regulatory networks in Drosophila eye development by large-scale transcriptome perturbations and motif inference. Potier D, Davie K, Hulselmans G, Naval Sanchez M, Haagen L, Huynh-Thu VA, Koldere D, Celik A, Geurts P, Christiaens V, Aerts S. Cell Rep. 2014 Dec 24;9(6):2290-303. doi: 10.1016/j.celrep.2014.11.038. Epub 2014 Dec 18.