We compare the claims of the C4ID with what is actually taught in a modern undergraduate biology degree
Not even a new claim
The claims made by the C4ID, despite their implications otherwise, are nothing new. They have a direct antecedent in the claims of William Paley in his book Natural Theology in 1802 where he made his famous “watchmaker”1 argument.
The claims made
The core of the C4ID argument as put forward by Dr. Alastair Noble is;
“In all our experience, information of this level of sophistication only comes from intelligent mind. It is therefore a thoroughly scientific position to infer that the information in living things comes from an intelligent source and in scientific jargon that means making the inference to the best explanation.”
He states this in the introductory video on the C4ID website, about which we are told, “The Director of the Centre for Intelligent Design, Dr Alastair Noble, introduces the Intelligent Design debate. . .”
So let’s look at this claim from the point of view of what modern science actually teaches. The Open University is world famous and teaches more people in more places than any other university in the world.
Mark Edon is one of our committee members and is half way through a BSc (Honours) in Life Sciences with the Open University and has just completed a course called Uniformity and Diversity2 which covers some aspects of this very question. Let’s look at what the well established and readily accessible science says and contrast it with Dr Noble’s claims.
This topic is covered in the text book “The Core of Life Volume 2” by Jill Saffrey (Ed), Melanie Clements, Jill Saffrey, Jane Loughlin, Judith Metcalfe, Ayona and Silva-Fletcher, of the Open University,
“Genetic change can be brought about by a variety of mechanisms. These include small mutations involving changes in base sequences; changes in chromosome structure or chromosome number; and recombination (crossing over and independent assortment) between chromosomes.”3
Let’s look at these mechanisms in turn, from a lay person’s point of view, and see if science does know anything on this topic, which Dr. Noble regards as so mysterious.
The chapter introduction alone lays out before us a complete rebuttal of Noble’s view as follows;
“Here, we shall study some of these topics, examining them in detail at the level of DNA, and explore additional mechanisms that bring about changes in the genome. Genetic change — whether by mutation or by recombination — provides variation that enables organisms to adapt to a changing environment, and hence it is fundamental to evolution. What has become clear from intensive studies of prokaryote and eukaryote genomes is that, over time, these processes have resulted in the evolution of complex genomes. In this chapter we shall describe how DNA mutation and recombination is linked with the gradual evolution of genomes.”3 pp345
The actual science
The chapter gives us details on the structure of DNA, how replication occurs and some of the modern techniques used to study DNA such as the “Polymerase Chain Reaction” and other sequencing techniques before going on to discuss mutation as follows:
“Mutations change the nucleotide sequence of DNA; they can be caused by a spontaneous damage event (resulting in chemical modification), a replication error or a mutagen (an agent that can cause mutation). Gene mutations that have a very subtle effect on a gene product are often a simple exchange of one base for another. More drastic changes may be caused by deletions or insertions of a nucleotide or a number of nucleotides.”3 pp359
Mutations can be characterised as one of the following types; transitions, transversions, frame-shifts and replication slippage. Each of these generates new information. We cannot understand why Intelligent Design advocates claim otherwise.
ID proponents only talk about mutations as being changes in individuals bases and then quote some rather off probability calculations to “prove” that such can never ever produce any changes that are useful. In fact many creationists make the point blank claim that all mutations are deleterious.
In this text book we instead get a discussion of the likelihood of gene mutation in the mouse genome;
“Even in cells with fully functioning repair mechanisms, errors occasionally go undetected or are not repaired, and so give rise to mutations. Therefore, it is interesting to consider the rate of mutation per gene, and the total amount of mutation in an organism that is uncorrected by the cell. As an example, we shall take a small mammal such as mouse for this calculation. The mutation rate can be estimated by observing the rate at which spontaneous genetic changes arise in a large population of mice, or by screening for changes in specific proteins in cells . . . grown in culture. Both methods suggest an uncorrected error frequency of one base-pair change in 109 bp for each cell generation. Consequently, a single gene of 103 coding base pairs would suffer a mutation once in about 106 (i.e. 109/103) cell generations. Something of the order of 1012 cell divisions take place in the lifetime of a mouse. Thus, on average, every single gene would have undergone mutation on about 106 (i.e. 1012/106) occasions. The older the mouse, the greater the total number of somatic mutations in the body. This conclusion is true for all organisms.”3 pp365
As it is then pointed out in the text, when such a mutation changes the reproductive success of an individual that carries it, the mutation will be subjected to natural selection.
“An individual carrying a particular mutation that leads to fewer than average progeny will decline in frequency.
What would happen to a rare variant gene sequence that increases the average number of progeny?
It would spread by natural selection.
Consequently, the structure and function of genes are refined by mutations, and mutations provide the raw material for evolution.”3 pp 365
Next we learn about another type of genome change, that resulting from recombination by crossing over. This is a process which happens during the formation of sperm or egg cells in humans and can result in huge diversity by effectively mixing existing genes. However it can also go awry resulting in the generation of new information.
Transposons generate several kinds of effects; insertions and frame shifts produce mutations, replicative transposition increases the genome length, the presence of multiple copies of transposons can result in the initiation of crossing over that can lead to exchange of genes between chromosomes that would not otherwise cross over.
The textbook continues:
“. . . we explore how the genome can evolve to become increasingly more complex as a result of the combined effects of recombination and mutation.
By comparing the genomes of different organisms, we can infer patterns of genome evolution that have occurred in the past. This section explores one such pattern, namely, how the genome can expand by means of duplications; we consider both coding sequences and non-coding sequences. Evidence of genetic change over evolutionary time again reveals how genomes are dynamic entities.
Many genes in higher eukaryotes belong to a gene family — in other words, a set of genes containing identical or closely related nucleotide sequences. It is possible to trace the evolution of a gene family from a single ancestral gene by comparing the DNA sequences of its individual members. First we explore the origins of members of a gene family; second we look at the functions of members of such families; third we review the evidence that members of a family arose by gene duplication and divergence. Finally, we examine non- coding DNA and genome evolution.”3 pp375
First up is the expansion of gene numbers by unequal crossing over.
“Initially, the two genes would have indistinguishable activities, but mutations in one of the duplicated genes could be tolerated because the other copy would still be able to carry out the original function. Thus, duplications produce additional genetic material capable of evolving new functions.”3 pp376
Evolution of new genes then gets an extra helping hand such gene duplicates themselves generate as stretches of such duplicated information make it more likely that such tandemly repeating genes cross over in future.
Next we get a glimpse of part of the huge pile of evidence that exists which supports the theory of evolution.
The diagram shows a scheme for the evolution of the oxygen-carrying proteins in vertebrates.
This agrees with the relationships seen in these organisms based on data from others fields. If evolution were not true then there would be no reason why this should be so - unless the “intelligent designer” wanted these creatures to look like they evolved.
Next this textbook takes us through the two key lines of evidence that support the theory that the globin genes evolved in this way;
“Evidence that the β-globin gene cluster arose by repeated duplication and divergence is provided by a comparison of nucleotide sequences within gene families and between species. Although exon sequences remain closely related, intron sequences vary, and may even be quite unrelated. Further evidence that the two globin gene clusters arose by repeated duplication comes from the study of genes that cause the human disease thalassaemia.”3 pp 383
Just as an interesting aside at this point, you may be familiar with the common claims made by creationists that , unlike Darwinians they predict that “junk DNA” will have a function. Well, here is real science on the subject;
“But what is the role of non-coding DNA? The presence of extensive amounts of it in eukaryote genomes (Figure 8.11) is still a puzzle for molecular biologists.One possibility is that the non-coding DNA has no function but is tolerated by the genome because of the absence of selective pressure to lose it. Another possibility is that non-coding DNA has a range of functions that so far have eluded molecular biologists. It is also possible that it has a completely different type of role in genome organization. Some of it at least has a physical role, such as the telomeres which protect the ends of chromosomes (Figure 8.4) and the centromeres, which are also composed of repetitive DNA, and which play a role in the separation of chromatids during mitosis (Chapter 7).”3 pp 383
Finally we are told about another feature of DNA that further explains the generation of new information. Protein domains and exon shuffling.
Functional proteins are made from amino acid sequences, the content of which is taken from the DNA sequence. Such DNA sequences are not continuous but consists of exons (coding for bits of the gene) interspersed with introns (non-coding sequences).
A domain is a structural unit of a protein. A part of the overall protein and sometimes we see that these domains correspond to the exons of the gene.
This means that any of the mechanisms we have already discussed that might result in a shuffling of the exons can lead to a new protein.
“The appearance of related exons in different genes support the important hypothesis: many genes are assembled from exons whose products perform particular functions.
It is believed that the organization of DNA coding sequences as a series of exons separated by longer introns has greatly facilitated the generation of new proteins.”3 pp 386
As a last word from this excellent text book a little bit of scientific humility;
“It is impossible to devise experiments that would prove that many genes have been assembled from combinations of exons encoding proteins that successfully perform particular functions. However, as seen in this chapter, the processes of gene duplication, exon duplication and transposition do occur, and combinations of these processes could bring about exon shuffling.” 3 pp 387
3 The Open University publication “The Core of Life Volume 2” 2nd Edition 2007, Jill Saffrey (editor) chapter 8, “DNA and Genome Evolution”
This article and others is available from BCSE Downloadable Resources in the leaflet entitled "Information Argument Exposed".