Note: this was originally written in late August 2005 in response to two correspondents. Some edits were made for clarity. What elicited that correspondence was the following:
So prevailing is the logic of nonrandom variation that I was at first flabbergasted in my failure to find any biologists working today who still believe mutations to be truly random. Their nearly unanimous acknowledgment that mutations are “not truly random” means to them (as far as I can tell) that individual mutations may be less than random — ranging from near-random to plausible; but they still believe that statistically, over the long haul, a mass of mutations behaves randomly. “Oh, randomness is just an excuse for ignorance,” quips Lynn Margulis.
This weak version of nonrandom mutation is hardly even an issue anymore, but a stronger version is more of a juicy heresy. It says that variations can be chosen in a deliberate way. Rather than have the gene bureaucracy merely edit random variations, have it produce variations by some agenda. Mutations would be created by the genome for specific purposes. Direct mutations could spur the blind process of natural selection out of its slump and propel it toward increasing complexity. In a sense, the organism would direct mutations of its own making in response to environmental factors. Ironically, there is more hard lab evidence at hand for the strong version of directed mutation than for the weak version.
According to the laws of neodarwinism, the environment, and only the environment, can select mutations; and the environment can never induce or direct mutations. In 1988 Harvard geneticist John Cairns and colleagues published evidence of environmentally induced mutations in the bacterium E. coli. Their claim was audacious: that under certain conditions the bacteria spontaneously crafted needed mutations in direct response to stresses in their environment. Cairns also had the gall to end his paper by suggesting that whatever process was responsible for the directed mutations “could, in effect, provide a mechanism for the inheritance of acquired characteristics” — a bald allusion to Darwin’s rival-in-theory Jean-Baptiste Lamarck.
Another molecular biologist, Barry Hall, published results which not only confirmed Cairns’s claims but laid on the table startling additional evidence of direct mutation in nature. Hall found that his cultures of E. coli would produce needed mutations at a rate about 100 million times greater than would be statistically expected if they came by chance. Furthermore, when he dissected the genes of these mutated bacteria by sequencing them, he found mutations in no areas other than the one where there was selection pressure. This means that the successful bugs did not desperately throw off all kinds of mutations to find the one that works; they pinpointed the one alteration that fit the bill. Hall found some directed variations so complex they required the mutation of two genes simultaneously. He called that “the improbable stacked on top of the highly unlikely.” These kinds of miraculous change are not the kosher fare of serial random accumulation that natural selection is supposed to run on. They have the smell of some design.
Both Hall and Cairns claim that they have carefully eliminated all other explanations for their results, and stick by their claim that the bacteria are directing their own mutations. However, until they can elucidate a mechanism for the way in which a stupid bacterium can become aware of which mutation is required, few other molecular geneticists are ready to give up strict Darwinism.
Wednesday, 31 August 2005
The Git is profoundly suspicious of the reductionist approach to biology. That is not to say he thinks it is incorrect, just that reductionism’s not the only path to understanding things. So the story goes, biology is reducible to chemistry, and chemistry is reducible to physics. That’s not to mention psychology being reducible to sociology and sociology being reducible to biology. Here’s the classical imagery:
Species (specific kinds of something) in chemistry are readily identified: hydrogen has one proton, helium two protons, lithium three protons… Claiming that while iron was a species because its atomic number is 26 and that there are other, different elements with the same atomic number, or that some elements are defined without regard to their atomic number is irrational. Yet in biology this is precisely what we do in order to “make sense” of species. Be aware that The Git isn’t arguing against any concept of species in biology, just that there are several different ways and that each has its merits and faults. On that account, we can for the purposes of a particular intellectual exercise adopt one or another, rather than insisting on a one-size-fits-all approach. This is likely what Kim Sterelny means and The Git certainly means when advocating pluralism. It seems that this is just because biology, unlike physics and to a lesser extent chemistry, is an infant science. Geology is also burdened by a plethora of conflicting theories and definitions. It’s notable though that geologists seem to be far less wedded to their theories and seem to welcome, rather than reject, forthcoming better theories!
It has been shown mathematically that a variant gene will tend to be rapidly lost from a large gene pool. In a restricted gene pool, gene variants have a much better chance of spreading throughout the population and surviving. The two criteria, reproductive isolation and a small gene pool, are met by the Galapagos tortoises. Thus the claim that they are well on the way to speciation is better grounded than any such claim for a group as large as the herring gulls. Here’s a map of the distribution of the world’s most numerous gull:
This was responding to the claim that the ring-species, herring gulls, was an example of speciation in progress.
Gould and Eldridge invoked the small isolated gene pool for their notion of punctuated equilibrium, an attempt to explain the lack of gradualism in the fossil record predicted by Darwinism. It remains the case that species tend to remain static for millions of years without any noticeable speciation. New species arise suddenly in the fossil record, not gradually. This is explicable if the isolated population remains very small while it undergoes evolutionary change by accumulated mutations. Environmental change then allows the new species to take advantage of the change and rapidly increase in population.
A further problem with the herring gulls is that their reproductive isolation appears to be due to behavioural differences; i.e. mate choice. While mate choice has to be at least partially genetically determined, it is by no means the case that it must be entirely genetic. It seems reasonable to assume that like many other species of animal, the young are imprinted by their parents. Any animal failing to sufficiently resemble the parental imprint would be rejected as a potential mate. An example of this sort of behaviour occurs with livestock kept for milking. There was something very touching about being groomed by the goats we milked. They clearly perceived us to be at least kid-like, though not necessarily identical to their biological offspring.
The herring gull population because it is so large and spread over a diverse range seems to be a prime candidate for stasis, rather than being in any process of speciation. The variations between different groups of herring gull appear to be directly analogous to those between varieties of dog. The Git notes here that even very small isolated gene pools do not guarantee speciation. There are at least two separate colonies of that rather rare fish, the coelacanth, for a long time believed extinct. Any explanation of speciation based on small, isolated gene pools must also explain the coelacanth and any other similar static species.
It’s problems such as we are discussing that lead to phylogenetic species concepts as a solution. Unfortunately, that leads to yet another can of worms. The problem is that it has proven just as difficult to define what a gene is. While researchers after Mendel had shown that certain phenotypic characteristics were linked to particular gene sequences, many are not. Some are the result of interactions of genes. Some genes are activated, or inactivated by the cell environment. Genes are defined by the nucleotide sequence between start and stop codons, but the relationship between them and phenotypic characteristics is not one to one, or even one to many. It’s many to many.
Let’s consider Susumu Ohno’s explanation [borrowed from Brig Klyce] of how random genetic mutation leading to new genes must occur. He wrote that for a new gene to evolve by mutation, an existing gene must be duplicated, become silent for a time, and undergo what he called “forbidden mutations”. The reasoning is that when we have pushed up the random mutation rate for organisms by artificial means, such as the many experiments with the fruit fly (drosophila), the results have generally been deleterious — bizarre even. Drosophila can be induced to grow fully formed legs from their eyes and, as you point out, extra wings that impede flying. Clearly, an organism cannot forego the utility of a gene while it mutates into something useful.
While silent, a gene cannot be improved, or even maintained, by natural selection. Rather, natural selection might tend to weed such silent genes out because they have no value to the organism. Remember that there’s nothing about random mutation to suggest that a single nucleotide substitution must take place. It seems just as likely that nucleotides could be lost, or added. If nucleotide sequences have any tendency to spontaneously grow in size, there appears to be little evidence for it.
Lenski’s Phenotypic and Genomic Evolution is a fairly accessible account of a 30,000 generation experiment with Escherichia coli, though only 20,000 generations had been analysed at the time of publication. The results were that the bacteria adapted to their environment, but there’s no evidence of evolution of novel characteristics that might indicate a progress toward more complex organisms. In other words, they remained staunchly Escherichia coli.
To arrive at a substantially different nucleotide sequence, many mutations are needed. These mutations would have to randomise the original sequence of the gene such that it loses its original meaning in order to qualify as having a new meaning. Ohno’s hypothesis sidesteps the problem of how a mutating gene would have to retain meaning while transforming into something with new meaning.
As any fule knows, a random nucleotide strand as long as an average gene has an absurdly high number of possible sequences. Assuming an average gene is 1,000 nucleotides long, the number of possible sequences it can have is 4^1000, or about 10^600. The chance of finding any gene currently expressed anywhere in biology in that sequence space, in even 10^50 trials, is less than 10^-500.
There are arguments to circumvent this problem, but they entail making stasis in organisms (such as the coelocanth) difficult to explain. It’s not clear how a gene can go silent, remain unaffected by natural selection while it undergoes a series of random mutations that just happen to randomly generate a novel and useful characteristic that then fortuitously becomes expressed. Recent research indicating rapid evolution of the human brain poses an even greater problem when it involves hundreds, possibly thousands of such nucleotide sequences all undergoing change virtually simultaneously. Clearly it’s not impossible, but anyone with an understanding of chance must find this all very hard to swallow. It’s not impossible for The Git to win first prize in the lottery several weeks in a row, but he’s not holding his breath waiting for such an occurrence…
There are at least four possible explanations here:
- It’s all just down to an amazing long streak of lucky events. We Know The Truth. Live with it. [neoDarwinists]
- This is not the explanation for evolution. Evolution involves whole nucleotide sequences (horizontal gene transfer). [Panspermia advocates/Margulis et alia]
- There is some undiscovered mechanism/mechanisms operating to skew the odds. That is, the process is not random at all. [Prigogine et alia]
- God done it.
Typically, the evidence for the neoDarwinist explanation takes a form similar to this:
“Peter and Rosemary Grant, two British-born researchers who have spent decades where Charles Darwin spent weeks, have captured a glimpse of evolution with their longterm studies of beak size among Galapagos finches.”
[Was Darwin Wrong? NO, the evidence for Evolution is overwhelming by David Quammen, National Geographic November 2004]
And because Natural Selection affects beak size within a species, it must therefore also be responsible for the differentiation between the formation of feather, human skin cells, or reptilian scales, i.e. marks of speciation. There is a huge difference between the rate at which a process takes place and the generation of new, previously non-existent functions. One wonders about how stupid they think we are.
During the last four billion years, or so, life on Earth evolved from prokaryotic single cells to eukaryotic single cells, to multicellular plants and animals. The increasingly complex suite of organs, systems, and features required an increase in the size and complexity of the genetic code. It should be clear that the evolution of entirely new organs, systems, or features requires new genes, not ever-so-slightly mutated versions of pre-existing genes.
Speciation through the introduction of new genes by horizontal gene transfer (HGT) is well documented although its existence is denied by that great populist for neoDarwinism, Richard Dawkins. HGT also explains what would otherwise be the “miraculous” invention of the C4 photosynthetic process in over thirty unrelated plant species in the neoDarwinist dogma. For example, “in August 1996, Carol J. Bult et al. reported sequencing the complete genome of the archaebacterium M. jannaschii. Among the genes it contains are, surprisingly, five histone genes (Morell). Histones are known to be used by eukaryotes as scaffolding for their complex chromosomal structure. Prokaryotes’ chromosomes do not have this structure and do not use histones.” While it might barely be possible for a bacterium to generate a single gene for which it has no use through random mutation, five such chance occurrences stretches credulity to the limit.
We might be tempted to ask whether there are any known examples of non-random mutation. Escherichia coli bacteria, it seems, do precisely that according to B G Hall, Department of Biology, University of Rochester, NY:
“Selection-induced mutations are nonrandom mutations that occur as specific and direct responses to environmental challenges and primarily in nondividing cells under conditions of intense prolonged selection. Selection-induced mutations have been shown to occur at six loci in Escherichia coli, but their existence has not previously been demonstrated in any eukaryotic organism. Here it is shown that selection-induced mutations occur at the HIS4 locus in the eukaryotic microorganism Saccharomyces cerevisiae.”
Some of the evidence at least appears to point toward bacteria being a source of new genetic codes and that bacteria can generate new codes through non-random mutation by as yet unexplained processes. Note that the bacteria were mutating at specific loci for a specific response to the environment in which they found themselves. While we can shun the term design, it certainly looks and smells purposive, and the very opposite of chance.
Some researchers believe that many biological processes have a quasi-mathematical relationship with non-living, self-organising processes. Self-organization refers to a process in which the internal organization of a system, normally an open system, increases automatically without being guided or managed by an outside source. Self-organizing systems typically (though not always) display emergent properties. Biologist Jack Cohen’s co-writer, Ian Stewart has written a book about the mathematical aspects of biology: Life’s Other Secret. The Git highly regards their books: The Collapse of Chaos and their later tome: Figments of Reality.
Susumu Ohno’s collaboration with his musician/wife Midori opens the door to some intriguing speculation:
In 1986, at 58, S. Ohno made one of his most interesting and popular discoveries. He published a paper in Immunogenetics examining the relationship between patterns of genetic sequence data and musical structure. He argued that using this similarity, the flood of genetic data since humans find meaning in music, but not in (seemingly) random sequences of letters. Basically, he found that when music was set to genes or genes set to music some strange things happen.
“The SARC oncogene, a malignant gene first discovered in chickens, causes cancer in humans as well. When Ohno translated the gene into music, it sounded very much like Chopin’s Funeral March. “An enzyme called phosphoglycerate kinase, which breaks down glucose, or sugar, in the body revealed itself to Ohno as a lullaby.”
He translates genes into music by assigning notes according to molecular weights. His ultimate goal is the discovery of some basic pattern (melody?) that governs all life. Not too long ago the motions of the planets were supposed to conform to an esthetically pleasing Music of the Spheres.
Ohno found a way to express the Music of the Genes. do to cytosine, re and mi to adenine, fa and so to guanine, and la and ti to thymine. Then, having assigned musical notes to each base, Dr. Ohno chose a particular key and timing, as well as the duration of each note. The result was a melodic composition that was finally fleshed out with harmonies by his wife, Midori, a musician. When completely transcribed, the scores were then performed by professional musicians on instruments such as the piano or organ, violin and viola.
Dr. Ohno notated over fifteen songs of the DNA of a variety of living organisms. He finds that the more evolved an organism is, the more complicated is the music. The DNA of a single-cell protozoan, for example, translates into a simple four-note repetition. But the music transcribed from human DNA — e.g., the body’s receptor site for insulin — is much more complex. Listeners knowledgeable about music have taken these DNA-based compositions for the music of Bach, Brahms, Chopin and other great composers.
As any dairy farmer can tell you, cows respond to music, becoming calmer when certain music is played in the milking shed and that the “wrong” type of music has unwanted effects. The Git also finds much Post-Modern, random music irritating. This should not be construed as a criticism of all Post-Modern composers. Philip Glass, Gavin Bryars and Michael Nyman all appear to create non-random and pleasant Post-Modern music.
It has been suggested that The Git must provide an explanation for giving any credence whatsoever to the possibility of Intelligent Design. He searched in vain for any online account of Richard Swinburne’s Argument from the Fine-Tuning of the Universe. It relies on a Bayesian statistical analysis of the Anthropic Principle. But he did find the following by the Christian physicist, James Hannam:
The Internet Infidels have long been interested in publishing a theistics defense of the fine-tuning argument against our criticisms, which are collected among our many essays on the Design Argument in general. James Hannam is the first to oblige, and the following essay is his defense of the Fine Tuning Argument for a creator. The Internet Infidels will respond in a forthcoming essay by Richard Carrier.
Of the traditional arguments for God, the teleological or design argument has recently enjoyed a new lease of life after many years out of favour. The classical formulation comes from Natural Theology, a book by William Paley published in 1802, in which the author asks us to compare living things to a watch he has found on the common. Because we can all agree that a watch is purposefully designed to tell the time, we should be equally able to conclude that plants and animals are purposefully designed to survive in each of their particular habitats. The argument is far older than that and appears in different forms in the work of both St Thomas Aquinas and Rene Descartes. Charles Darwin put paid to this formulation of the argument in 1859 with his theory of evolution which explained how living things came to be. All was quiet on this front for some time, but today teleology is back in fashion as an argument from the fundamentals of physics and, less successfully perhaps, biology. This essay outlines the new argument from design based on the fine tuning of the laws of physics.
One thing a design argument must not do is look for a ‘God in the Gaps.’ That is to say, we must not try and find theological explanations for scientific phenomena that science itself has not yet explained. The classic example of this is the origin of life on Earth. Many Christians have been beguiled by the idea that because life is so improbable, God must have actually stepped in to have created it. I reject this for two reasons–the first is that I do not think God, having created the universe for living creatures to live in, would have done such a bad job as to make it near impossible for such creatures to arise. Secondly, we are held hostage by the possibility (in my opinion, probability) that one day a science will create life in a test tube. Hence I feel Christians should avoid the origin of life in apologetics especially as I believe that many efforts in this field are misinformed.
And here is the rebuttal:
In his essay “In Defense of the Fine Tuning Design Argument” (2001) published here on the Secular Web, I do not believe Hannam has addressed the full range of issues and problems with the Fine Tuning Argument as discussed in our essays against the Design Argument. As but one example, he dismisses Victor Stenger’s “Monkey God” program as little more than “a bit of fun,” but this is a serious research product, defended at length in a technical article, “Natural Explanations for the Anthropic Coincidences,” Philo, 3:2 (Fall-Winter 2000) [click here for Acrobat/PDF version]. Hannam does not interact with this work at all. He thus does not consider that Stenger’s model varies all constants dynamically, not just one while keeping the others the same, and thus Monkey God generates a far more inclusive information space from which to judge relative probabilities. Hannam also criticises it for only addressing four rather than six constants, but in fact only four constants are relevant for generating long-lived stars, whose existence makes the conditions for life highly probable, regardless of what the other constants turn out to be, as Stenger argues in the above-mentioned paper. There are certain unjustified assumptions in Stenger’s argument (e.g. see point 3 below), but they are the very same assumptions Hannam and other creationists build upon.
However, Hannam correctly dismisses a great many theistic fallacies that our other essays have also refuted in more detail, and thus his position is more sound than most, and worthy of careful attention. But rather than pick on more specific examples like the Stenger case above, this essay will focus on some of the general, sweeping problems that Hannam’s essay does not resolve.
Quoting from further along in the refutation:
Framed this way, we see that Hannam has not made an adequate case for theism from the proposal of ‘fine tuning’, since we have no direct evidential support for any theistic hypothesis (all we have is the datum in need of explanation) and no evidence falsifying the nontheistic alternatives, which are not illogical, and whose improbability cannot be observed or known. Even if we reject the claim (made by many an expert) that we have direct evidential support for some nontheistic hypotheses, agnosticism (i.e. the conclusion that we do not know who is right) is still the only justified position, and that means Fine Tuning cannot support any argument for the existence of a Creator without commiting the fallacy of argumentum ad ignorantiam.
And a similar criticism applies to the case of neoDarwinism: “all we have is the datum in need of explanation… agnosticism (i.e. the conclusion that we do not know who is right) is still the only justified position.”
Thought for the Day
As my conclusions have lately been much misrepresented, and it has been stated that I attribute the modification of species exclusively to natural selection, I may be permitted to remark that in the first edition of this work, and subsequently, I place in a most conspicuous position — namely at the close of the Introduction — the following words: “I am convinced that natural selection has been the main, but not the exclusive means of modification.” This has been of no avail. Great is the power of steady misrepresentation. — Charles Darwin