Replies

10. Mutations are essential to evolution theory, but mutations can only eliminate traits. They cannot produce new features.
On the contrary, biology has catalogued many traits produced by point mutations (changes at precise positions in an organism’s DNA)—bacterial resistance to antibiotics, for example.

This is a serious mis-statement of the creationist argument. The issue is not new traits, but new genetic information. In no known case is antibiotic resistance the result of new information. There are several ways where an information loss can confer resistance—see Anthrax and antibiotics: Is evolution relevant? We have pointed out in various ways how new traits, even helpful, adaptive traits, can arise through loss of genetic information (which is to be expected from mutations). See for example, Beetle bloopers.

Mutations that arise in the homeobox (Hox) family of development-regulating genes in animals can also have complex effects. Hox genes direct where legs, wings, antennae and body segments should grow. In fruit flies, for instance, the mutation called Antennapedia causes legs to sprout where antennae should grow.

Once again, there is no new information! Rather, a mutation in the hox gene results in already-existing information being switched on in the wrong place. See also Hox (homeobox) Genes — Evolution’s Saviour? and Hox Hype — Has Macro-evolution Been Proven? The hox gene did not produce any of the information that results in the complex structure of the leg, which in ants and bees includes a very complex mechanical and hydraulic structure by which these insects stick to surfaces—see Startling stickiness.

These abnormal limbs are not functional, but their existence demonstrates that genetic mistakes can produce complex structures, which natural selection can then test for possible uses.

Amazing—natural selection can test for ‘possible uses’ of ‘non-functional’ (i.e. useless!) limbs in the wrong place. Such deformities would be active hindrances to survival.

Moreover, molecular biology has discovered mechanisms for genetic change that go beyond point mutations, and these expand the ways in which new traits can appear. Functional modules within genes can be spliced together in novel ways. Whole genes can be accidentally duplicated in an organism’s DNA, and the duplicates are free to mutate into genes for new, complex features.

Gene duplication, polyploidy, insertions, etc. do not help — they represent an increase in amount of DNA, but not an increase in the amount of functional genetic information—these create nothing new. Macroevolution needs new genes (for making feathers on reptiles, for example).

In plants, but not in animals (possibly with rare exceptions), the doubling of all the chromosomes may result in an individual which can no longer interbreed with the parent type—this is called polyploidy. Although this may technically be called a new species, because of the breeding isolation, no new information has been produced, just repetitious doubling of existing information. If a malfunction in a printing press caused a book to be printed with every page doubled, it would not be more informative than the proper book. (Brave students of evolutionary professors might like to ask whether they would get extra marks for handing in two copies of the same assignment.)

Duplication of a single chromosome is normally harmful, as in Down’s Syndrome. Insertions are a very efficient way of completely destroying the functionality of existing genes. Biophysicist Dr Lee Spetner in his book Not By Chance (see graphic, right) analyses examples of mutational changes that evolutionists have claimed to have been increases in information, and shows that they are actually examples of loss of specificity, which means they involved loss of information (which is to be expected from information theory).

The gene duplication idea is that an existing gene may be doubled, and one copy does its normal work while the other copy is redundant and non-expressed. Therefore it is free to mutate free of selection pressure (to get rid of it) . However, such ‘neutral’ mutations are powerless to produce new genuine information. Dawkins et al. point out that natural selection is the only possible naturalistic explanation for the immense design in nature (not a good one, as Spetner et al. have shown). The proposal is that random changes produce a new function, then this redundant gene becomes expressed somehow, thus comes under the selective process and is tuned.

It’s all a lot of hand-waving. It relies on a chance copying event, genes somehow being switched off, randomly mutated to something approximating a new function, then being switched on again so natural selection can tune it.

Furthermore, mutations do not just occur in the duplicated gene; they occur throughout the genome. Consequently, all the deleterious mutations have to be eliminated by the death of the unfit. Mutations in the target duplicate gene are extremely rare—it might represent only 1 part in 30,000 of the genome of an animal. The larger the genome the bigger the problem. This is because a larger the genome, the lower the mutation rate that can be sustained without error catastrophe, which means one has to wait longer for any mutation, let alone a desirable one, in the duplicated gene. There just has not been enough time for such a naturalistic process to account for the amount of genetic information that we see in living things.

Dawkins and others have recognised that the ‘information space’ possible within just one gene is so huge that random changes without some guiding force could never come up with a new function. There could never be enough experiments (mutating generations of organisms) to find anything useful by such a process. Note that an average gene of 1,000 base pairs represents 41000 possibilities — that is 10602 (compare this with the number of atoms in the universe estimated at ‘only’ 1080). If every atom in the universe were an experiment every millisecond for the supposed 15 billion years of the universe, this could only try a maximum 10100 of the possibilities. So such a ‘neutral’ process cannot find any sequence with specificity (usefulness), even allowing for the fact that there may be more than just one sequence that is functional to some extent.

So Dawkins and company have the same problem as the neutral selection theory advocates. Increasing knowledge of the molecular basis of biological functions has exploded the known ‘information space’ such that mutations and natural selection, with or without gene duplication, or any other known natural process, cannot account for the irreducibly complex nature of living systems.

Comparisons of the DNA from a wide variety of organisms indicate that this is how the globin family of blood proteins evolved over millions of years.

This is an inference from similarities interpreted under the materialistic paradigm. There is no actual demonstration that hemoglobin (with four polypeptides) evolved from myoglobin (with one polypeptide), or any adequate explanation of how the hypothetical intermediates would have had selective advantages. In fact, it’s far more complicated than Rennie implies. The a- and b-globin chains are encoded on genes on different chromosomes, so they are expressed independently. This expression must be controlled precisely, otherwise various types of a disease called thallassemia result. Also, there is an essential protein called AHSP (Alpha Hemoglobin Stabilizing Protein) which, as the name implies, stabilizes the a-chains, and also brings it to the b-chains. Otherwise the a-chains would precipitate and damage the red blood cells. AHSP is one of many examples of a class of protein called chaperones which govern the folding of other proteins.12 This is yet another problem for chemical evolutionary theories—how did the first proteins fold correctly without chaperones, and since the chaperones themselves are complex proteins, how did they fold? See The Origin of Life: A Critique of Current Scientific Models (PDF file).