A bit of background
Darwin (1809-82) envisaged that evolution proceeds gradually: small variations arise naturally, natural selection favours advantageous ones, and repeated accumulation of small improvements progressively leads to large-scale changes.
Darwin did not know why or how variations occurred, in The Origin of Species concluding that “Our ignorance of the laws of variation is profound”. He thought they might arise randomly, or speculated that they were caused somehow in response to an individual’s environment or way of life – somewhat similar to Lamarck’s acquired characteristics.
He also did not know how heredity works, in fact was quite baffled by some phenomena, such as why a characteristic could be present in both parents but not their offspring, or vice versa. In due course he decided in favour of some form of pangenesis, even though he knew this could not account for some observations.
In essence, the theory of pangenesis proposed that particles (gemmules) are formed in the tissues – their nature and/or number could be affected by the degree of use or fitness for purpose of the relevant organ – make their way to the gonads, and are then transmitted to the next generation, where gemmules from both parents are mixed, and they affect development of the relevant tissue.
Darwin also recognised that a problem with a blending mechanism is that (the gemmules related to) a favourable variation might be susceptible to being diluted in successive generations (through mixing with gemmules of a parent without the favourable variation), so this would counter the effect of natural selection.
Towards the end of the 19th century, August Weismann (1834-1914) made a major advance in the theory of heredity.
Mitosis had been observed since the 1870s; and, based on the elaborate way in which chromosomes are duplicated and then shared between daughter cells when cells divide, Weismann reasoned that the hereditary information is associated with the chromosomes. In addition, recognising that all of an organism’s tissues are derived by cell division from a fertilised egg, he deduced that all of the hereditary information in all of the cells of an organism is derived from the fertilised egg.
In fact he proposed that the flow of hereditary information is only one way – from fertilised egg to the tissues (including gonads) – and not from other tissues to the gonads e.g. by gemmules. So he drew the important distinction between the germ cells which pass on genetic information, and the somatic cells – those of the rest of the body – which did not contribute to the next generation’s hereditary information. Hereditary information is then passed from one generation to the next by the gametes produced in the gonads.
New variability arose not by acquired characteristics in the body as a whole (as Darwin had envisaged), but by random changes to the hereditary material in the germ cells. We take this view for granted now, but at the time it was a radical new way of thinking. The evolutionary biologist, and friend of Darwin, Georges Romanes (1848-94) coined the term ‘neo-Darwinism’ to refer to Darwinian evolution which took on board the key role of the germ cells in inheritance, rather than somatic cells.
At about the same time as Darwin was writing the Origin, Gregor Mendel (1822-84) was carrying out his breeding experiments with pea plants, which gave the first insight into the genetic basis of heredity. Unfortunately, although published in the 1860s, his work did not become widely known until 1900. Mendel’s work was a huge step forward in understanding how inheritance works. He showed that inheritance is mediated by discrete factors, which we now call genes.
However, this posed a challenge to Darwin’s evolution: the discrete nature of genes, and their effects, did not seem to be consistent with Darwin’s theory of gradual progress through a series of very small changes.
On the other hand, the discrete nature of genes avoided the problem posed by a blending mechanism – of advantageous variations being diluted – because provided the relevant gene is present it can have its full effect.
Nevertheless, the initial effect of discovering Mendel’s work was to cast doubt on Darwin’s theory of gradual evolution.
And at the beginning of the 20th century, as well as this question about gradual change, there were doubts about the efficacy of natural selection acting on small variations to bring about all the change that Darwin had envisaged or whether sometimes there would need to be mutations that have a substantial effect.
The new synthesis of evolution
In the early decades of the 20th century there were several key advances which resolved these queries, and the theory of evolution emerged all the stronger.
1. Genes were unequivocally identified with chromosomes.
Also, it was realised that the process of meiosis (observed in the late 19th century) was not only (a) the means for separating sets of chromosomes between parental gametes, but also (b) the crossing over of chromosomes in the course of meiosis (see figure) enables gametes to have different mixes of the available genes (derived from their parents), and hence offspring (even of the same parents) to have different mixes of the genes present in their parents.
2. Most species were found to have extensive genetic variability – far more than had been anticipated.
And, although Mendel’s experiments had been based on single genes having a discrete impact, it became apparent that many traits result from the interaction of many genes (and some genes affect multiple traits), such that some characteristics (e.g. height) can vary gradually over a wide range. So this meant that characteristics could vary in the gradual way that Darwin had envisaged.
This genetic variability – shuffled by meiosis – also means that most species can vary and hence evolve to a large degree. This includes adaptation to e.g. new environments, and speciation by segregating the available genes in different ways (selecting different subsets of the available genes /alleles). Fisher, a mathematician who played a major role in founding population genetics (see below) commented:
It has often been remarked, and truly, that without mutation evolutionary progress, whatever direction it may take, will ultimately come to a standstill for lack of further possible improvements. It has not so often been realised how very far most existing species must be from such a state of stagnation, or how easily with no more than one hundred factors a species may be modified to a condition considerably outside the range of its previous variation, and this in a large number of different characteristics. 
3. Significant mutations were observed.
These arose mainly from the work of Thomas Morgan (1866-1945) on the fruit fly Drosophila melanogaster. Using various means he induced a range of mutations affecting e.g. eye colour and wing size, and demonstrated that they were inherited. These discoveries were seen as indicating how evolution proceeds – heritable mutations arise, and favourable ones are the basis for natural selection to act and lead to gradual progress.
4. Population genetics was founded.
Darwin had focused on the evolution of individuals. However with the recognition that individuals do not acquire variations appropriate to their way of life, which can be passed on to progeny, but that mutations arise at random in the genetic material, which adds to the genetic variability within a species, it became apparent that individuals themselves do not evolve.
Rather, it is populations that evolve. A species’ population has genetic variability expressed as phenotypic variations. Individuals with favourable variations preferentially survive/reproduce, leading to an increase in the next generation of the genes responsible for the favourable variations. Consequently, evolution was increasingly seen as a change in gene frequencies within a population.
The mathematicians Ronald Fisher (1890-1962), J. B. S. Haldane (1892-1964) and Sewall Wright (1889-1988) were the key figures who developed mathematical models to describe how gene frequencies change in response to e.g. different levels of selective advantage and population size – and thus founded the discipline of population genetics. It was population genetics that finally brought together – a synthesis of – the Darwinian concept of natural selection with Mendelian genetics. And this revised formulation came to be known as the synthetic or modern theory of evolution, or Neo-Darwinism.
By the middle of the 20th century Darwinism had come through the major challenges of doubts about the efficacy of natural selection, and the capacity for gradual change, and was firmly established as the prevailing paradigm, or explanatory principle, of biology. Theodosius Dobzhansky (1900-75), who worked with Thomas Morgan and was one of the architects of the modern evolutionary synthesis, summed up the prevailing view when he wrote his well-known essay titled:
Nothing in biology makes sense except in the light of evolution.
Evolution and molecular biology
However, there is a negative aspect to this early triumph of Neo-Darwinism. Because of the success of the theory of evolution at the morphological and genetic levels it was widely believed that this proved evolution to be substantially true, and that any new knowledge would be consistent with and could be embraced by the theory.
In particular, evolution became the prevailing paradigm (see Thomas Kuhn, below) in biology before there was much knowledge about biology at the molecular level:
- even before it was known that proteins have a specific amino acid sequence (when Fred Sanger sequenced insulin in the 1950s);
- before the double helix structure of DNA was known (1953), and well before it was known how DNA codes for proteins, or the structure of genes (1960s);
- and long before we began to realise the sophistication and complexity of biological mechanisms at the molecular level e.g. how DNA is replicated or chromosomes are separated at cell division.
Because of the paradigm status of evolution there was a presumption that the discoveries of molecular biology would be entirely consistent with evolution, even to the extent that discoveries in molecular biology would not be allowed to challenge the fundamental tenets of evolution (again, see Thomas Kuhn).
A clear example of this entrenchment arose in a symposium that took place at The Wistar Institute of Anatomy and Biology, Philadelphia, in 1966.  This was perhaps the heyday of Neo-Darwinism, and the implications of molecular biology were just beginning to be appreciated. The symposium was specifically convened to enable leading evolutionists to discuss ‘Mathematical Challenges to the Neo-Darwinian Interpretation of Evolution’, so it was clear that the purpose of the meeting was to take these mathematical challenges seriously – they were not some sideline at a conference on another issue.
One of the mathematicians, Dr Stanislaw Ulam, presented a paper  in which he outlined various difficulties, especially of there not being enough time available for evolution to occur – even to accumulate a series of advantageous changes (i.e. not trying to get there in one jump, which had been the scenario of the preceding paper). In the following discussion, one of the biologists, Prof. C. H. Waddington, said:
You are asking, is there enough time for evolution to produce such complicated things as the eye? Let me put it the other way around: Evolution has produced such complicated things as the eye; can we deduce from this anything about the system by which it has been produced?
Followed by Sir Peter Medawar:
May I make a point here in support of what Waddington says? I think the way you have treated this is a curious inversion of what would normally be a scientific process of reasoning. It is indeed a fact that the eye has evolved; and, as Waddington says, the fact that it has done so shows that this formulation [i.e. the mathematical argument presented by Ulam] is, I think, a mistaken one.
And, in presenting the next paper, Ernst Mayr said that they should approach the subject from the point of view that evolution has happened.
These comments clearly illustrate what it means to be operating within a paradigm. For the biologists it was not a question of how good or bad the mathematical argument was – they did not consider that. As far as they were concerned their paradigm was true and they rejected anything that would not fall in line with it. Rather than allow anything to challenge their beliefs, their firm presumption was that there must be something wrong with the supposed challenge, even if they had no idea what it was. The symposium was convened specifically to consider mathematical challenges to Neo-Darwinism, but for the biologists it could be construed only as biological objections to the maths! 
Consequently, any discoveries that are consistent with evolution are eagerly seized upon as further confirming the truth of evolution.
An example of this are comparative amino acid sequences: for a given protein (notably cytochrome c which is present in almost all organisms), the sequence varies between species. In general, for species that are generally considered close to each other from an evolutionary perspective, e.g. mammals or plants, the sequences are similar; but for species that are further apart eg. mammals vs plants, the sequences are more different. Hence the divergence of protein amino acid sequences is seen as reflecting, in fact arising from, the evolutionary divergence of organisms.
But any discoveries that are not consistent with evolution are ignored, or ad hoc explanations are devised to accommodate the offending observations.
Most biology textbooks cite homology as evidence in favour of evolution. However, there are significant exceptions – where organs that appear to be homologous morphologically, are formed embryonically in substantially different ways, so they are not actually homologous (at least not in an evolutionary sense). These exceptions have been known for a long time, but are rarely mentioned. The more we learn about developmental biology at the molecular level, the more it is evident that early embryonic processes cannot be constructively modified (the ad hoc evolutionary way to explain away the anomalies), so the stronger is the case that these non-homologies refute common ancestry.
The issue I shall focus on here is that of new genes.
There is a very strong case against new genes arising in an evolutionary way, yet most (if not all) scenarios proposed for the evolution of e.g. eyes or wings, which must require new genes, completely ignore this fact. Almost invariably such scenarios consider only the morphological level, a notable example being Nilsson and Pelger’s proposed evolution of eyes.  This is a fundamental flaw which seriously undermines such scenarios.
I think there are several reasons for this oversight:
1. Out-of-date thinking about morphological plasticity
Partly it is for historical reasons. Darwin, being aware that morphological variations arise (but knowing nothing of genes, embryonic processes or molecular biology), in effect considered biological tissues to be plastic – able to vary freely. It was well known at the time that, whilst substantial morphological changes could be achieved by breeding, there was a limit. Darwin was of course aware of this, but thought that given time the powers of nature could transcend those limits; so he felt able to extrapolate beyond observable morphological change more or less indefinitely.
Then, in the first decades of the 20th century, biologists discovered the basis for observed morphological variations – the large genetic variability of most species. Also, the reason why morphological variations (e.g. through breeding) are limited – is because the available genetic variability, whilst substantial, is finite. And as Richard dawkins wrote (excuse my using this quote again!):
If anything, selective breeders experience difficulty after a number of generations of successful selective breeding. This is because after some generations of selective breeding the available genetic variation runs out, and we have to wait for new [useful] mutations. 
Professional biologists know this very well, and yet persistently ignore it in putative evolutionary scenarios. They assume that the morphological variation possible through existing genetic variability can be extended indefinitely – given enough time and the powers of nature / evolution. In effect – if they think about it at all – they assume that such genes as may be necessary will arise as required and their effect blend seamlessly with that of those already present.
At least Dawkins is fairly clear about this. In The Blind Watchmaker, in the section where he is considering questions about whether his model for the evolution of an eye (via a series of intermediates he calls Xs) is plausible, he writes:
4. Considering each member of the series of hypothetical Xs connecting the human eye to no eye at all, is it plausible that every one of them was made available by random mutation of its predecessor?
This is really a question about embryology, not genetics; … Mutation has to work by modifying the existing processes of embryonic development. It is arguable that certain kinds of embryonic process are highly amenable to variation in certain directions, recalcitrant to variation in others. … The smaller the change you postulate, the smaller the difference between X” and X’, the more embryologically plausible is the mutation concerned. In the previous chapter we saw, on purely statistical grounds, that any particular large mutation is inherently less probable than any particular small mutation. Whatever problems may be raised by Question 4, then, we can at least see that the smaller we make the difference between any given X’ and X”, the smaller will be the problems. My feeling is that, provided the difference between neighbouring intermediates in our series leading to the eye is sufficiently small, the necessary mutations are almost bound to be forthcoming. We are, after all, always talking about minor quantitative changes in an existing embryonic process. Remember that, however complicated the embryological status quo may be in any given generation, each mutational change in the status quo can be very small and simple. 
The logic sounds convincing – make any change small enough and the probability it will arise will be good enough to be fairly sure it will happen. However (as I elaborate in my critique of The Blind Watchmaker), Dawkins’ rationale fails because of the discrete nature of genes, coupled with the fact that genes cannot arise in a gradual progressive way – through ‘very small and simple’ mutational changes (see hurdles to new genes).
To put it another way, although Dawkins sees any advance as ‘always … about minor quantitative changes in an existing embryonic process’, at least for significant new structures – those requiring new genes (and usually many acting in concert), not just modified ones – these constitute quantum or qualitative changes. (For an example see my critique of Nilsson and Pelger.)
It seems to me that in the above passage Dawkins expresses the implicit assumption behind most scenarios for the proposed evolution of new organs. But in fact this is the Achilles heel of any evolutionary scenario that considers only the morphological level – which is most of them.
Is this just an oversight through not thinking clearly enough about what is going on, or a more deliberate omission because biologists know that to look closely will expose a fatal flaw in the theory of (macro)evolution?
2. The existence of mutations that affect morphology.
Prominent among these are of course those affecting Drosophila such as the ones mentioned above. At the time these were seen as illustrating the sort of beneficial mutations – or at least introducing genetic variability – that fuelled long-term evolution. We now know that these morphological mutations arose through deactivating genes, not from creating new ones (see Phenotypic variations caused by corrupting genes) yet the belief seems to persist that there is evidence for the constructive mutations resulting in the new genes that evolution would require.
It is firmly believed that the overall evolutionary account – from the earliest organisms (or even before) to higher plants and animals – is substantially true. Such evolution requires that new genes must have arisen along the way; so even if there appear to be obstacles and we can’t see how genes might have arisen, this is not a reason to reject evolution, but rather a puzzle  that can be the subject for further scientific research.
Notes display in the main text when the cursor is on the Note number.
1. Charles Darwin (1968, first published in 1859), The Origin of Species, Penguin Classics edition, Penguin Books, p222.
2. Jean-Baptiste Lamarck, see Wikipedia article 'Inheritance of acquired characteristics'.
3. See Wikipedia article 'Pangenesis'.
4. See Wikipedia article 'Mitosis'.
5. Initially it was thought to be with their protein content; not until the 1940s was it known to be the DNA.
6. See Wikipedia article 'Meiosis'.
7. Ronald Fisher (1958, first published 1929), The Genetical Theory of Natural Selection, Revised edition, Dove Publications Inc., p103.
8. Thomas Kuhn (1996, first published 1962), The Structure of Scientifc Revolutions, 3rd edition, University of Chicago Press, 1996, p5.
9. The Wistar Institute (1967), Mathematical challenges to the Neo-Darwinian interpretation of evolution, Symposium 25-6 April 1966, Wistar Institute Symposium Monograph No.5, Wistar Institute Press.
10. Stanislaw Ulam (1967), 'How to formulate mathematically problems of rate of evolution', in .
11. David Swift (2002), Evolution under the microscope, Leighton Academic Press, p371.
12. Dan-E Nilsson and S Pelger (1994), 'A pessimistic estimate of the time required for an eye to evolve', Proc. Royal Soc. Series B, London 256, p53-8.
13. Richard Dawkins (1991, first published 1986), The Blind Watchmaker with Appendix, Penguin Books, chapter 9, p247; italics in the original.
14. Richard Dawkins (1991, first published 1986), The Blind Watchmaker with Appendix, Penguin Books, chapter 9, p76; italics in the original, underlining added.
15. This is Kuhn's word to describe how scientists working within a paradigm view observations that do not seem to be consistent with the paradigm.
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Page created March 2017, last revised on 18 May 2017.