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J. G. Mendel: Why his discoveries were ignored for 35 (72) years?


Some critical comments about the effects of Darwinism on Biological Research by Pioneers of Genetics as well as further Biologists and Historians of Biology.

Especially in the decade after the publication of Darwin’s ORIGIN (1859) the scientific world was eagerly awaiting the discovery of the laws of heredity by some experimental or other scientist(s). After two lectures in 1865, Mendel published his famous Pisum-treatise VERSUCHE ÜBER PFLANZEN-HYBRIDEN in 1866. His work was quoted at least 14 times before 1900, the year of its ‘rediscovery’. There were references in such widely distributed works as Focke’s DIE PFLANZEN-MISCHLINGE (1881), THE ENCYCLOPAEDIA BRITANNICA (1881) and the CATALOGUE OF SCIENTIFIC PAPERS OF THE ROYAL SOCIETY (1879).The treatise had been sent to the libraries of some 120 institutions including the Royal and Linnean Society of Great Britain. Moreover Mendel had 40 additional reprints at his disposal, many of which he sent to leading biologists of Europe. In fact, professor Niessl (1903 and 1906) emphasized that Mendel’s work was “well known” at his time. So in the face of the expectations just mentioned, – why was the discovery of the laws of heredity ignored by most scientists for more than 35 years, until 1900, and by the “true Darwinians” (Mayr) for another 37 years? That is 72 years in all!

The reasons have been hinted at or clearly stated by several pioneers of genetics as de Vries (1901), Bateson (1904, 1909, 1924), Johannsen (1909, 1926) as well as several historians of biology and/or biologists as Niessl (1903, 1906), Richter (1941, 1943), Stern (1962), Lönnig (1982, 1986, 1995), Callender (1988) and Bishop (1996):

All the evidence points to the main reason as follows: Mendel’s ideas on heredity and evolution were diametrically opposed to those of Darwin and his followers. Darwin believed in the inheritance of acquired characters (and tried to back up his ideas with his pangenesis hypothesis, which even Stebbins called an “unfortunate anomaly”) and, most important of course, continuous evolution. Mendel, in contrast, rejected both, the inheritance of acquired characters as well as evolution. The laws discovered by him were understood to be the laws of constant elements for a great but finite variation, not only for culture varieties but also for species in the wild (Mendel 1866, pp. 36, 46, 47). In his short treatise EXPERIMENTS IN PLANT HYBRIDIZATION mentioned above Mendel incessantly speaks of “constant characters”, “constant offspring”, “constant combinations”, “constant forms”, “constant law”, “a constant species” etc. (in such combinations the adjective “constant” occurs altogether 67 times in the German original paper). He was convinced that the laws of heredity he had discovered corroborated Gärtner’s conclusion “that species are fixed with limits beyond which they cannot change”. And as Dobzhansky aptly put it: “It is…not a paradox to say that if some one should succeed in inventing a universally applicable, static definition of species, he would cast serious doubts on the validity of the theory of evolution”.

As the Darwinians won the battle for the minds in the 19th century, there was no space left in the next decades for the acceptance of the true scientific laws of heredity discovered by Mendel and further genetical work was continued mainly by Darwin’s critics among the scientists. In agreement with de Vries, Tschermak-Seysenegg, Johannsen, Nilsson, et al., Bateson stated (1909, pp. 2/3):

“With the triumph of the evolutionary idea, curiosity as to the significance of specific differences was satisfied. The Origin was published in 1859. During the following decade, while the new views were on trial, the experimental breeders continued their work, but before 1870 the field was practically abandoned.

In all that concerns the species the next thirty years are marked by the apathy characteristic of an age of faith. Evolution became the exercising-ground of essayists. The number indeed of naturalists increased tenfold, but their activities were directed elsewhere. Darwin’s achievement so far exceeded anything that was thought possible before, that what should have been hailed as a long-expected beginning was taken for the completed work. I well remember receiving from one of the most earnest of my seniors the friendly warning that it was waste of time to study variation, for “Darwin had swept the field“” (emphasis added).

The general acceptance of Darwin’s theory of evolution and his ideas regarding variation and the inheritance of acquired characters are, in fact, the main reasons for the neglect of Mendel’s work, which – in clear opposition to Darwin – pointed to an entirely different understanding of the questions involved (see above).

However, the idea of Bishop (1996) and Di Trocchio (1991) as to Mendel that “most of the experiments described in Versuche are to be considered fictitious” or “…we are today forced by a series of anomalies and incongruities to admit that Mendel’s account of his experiments is neither truthful nor scientifically likely, and that the strategy he really followed must have been completely different” (Di Trocchio 1991, p.487 and p. 491, emphasis added) is in my opinion for several reasons untenable. (1) It does not match Mendel’s character which is distinguished by humility, extreme modesty and accuracy in handling things. (2) Too much is known about his life, work and correspondence to simply deny the existence of the work he has described (see the publications of Orel, Stern, Weiling and many others). (3) Fisher’s claims of fraud in Mendel’s data have already been disproved by several geneticists and historians of biology (Lamprecht 1968, Pilgrim 1986, Weiling 1995, Vollmann and Ruckenbauer 1997, and many other authors, see below). Working with Pisum for 7 years, I myself have found very similar data for several characters as Mendel had. In an answer to Edward, Ira Pilgrim commented (1986, p. 138): “…one had better have a good deal more evidence (such as a set of loaded dice or perhaps the information that the man is a known cheat) before accusing someone of cheating, which is what Fisher did to Mendel, and those who cite Fisher are doing now.”

On the other hand, if not only the accusations of Fisher but also those of Di Trocchio and Bishop were true, they would make Mendel’s work one of the greatest hoaxes in the whole history of science (“he counted 19,959 individuals” etc., Zirkle) – and at the same time the most ingenious fiction ever produced: an invention hitting directly upon the truth of the laws of heredity with many basic repercussions on nearly all biological and medical areas and our understanding of the living world. However, as long as there are no real foundations for these suspicions and as long as no convincing proofs can be advanced, – proofs which could stand the test of any honest court trial, the accusations fall back on those who produce them: fiction, invention and/or lies in the minds of the inventors (according to A. Kohn, Mendel belongs to the “false prophets”, M. Gardner states that “even Brother Mendel lied” (emphasis added) and V. Orel (1996, p. 207) lists further such examples).

The more I ponder and test the accusations regarding Mendel’s works, the more improbable and absurd the accusations appear to me, and the question comes to my mind: Could it be that now – after the creation position of a scientific giant like Mendel has become clear to so many observers – these accusations are the last resort of a more or less unconscious method of evolutionary philosophy to discredit Mendel and his work after all? 

Hubert Markl comments on the accusations of dishonesty against some renowned scientists (1998, p. VII): “Even if Galilei, Newton or Mendel had cheated when presenting the reasons and evidence for the natural laws they had discovered, that which they had recognized as being true, is nevertheless true, because it was found to be right in multiple tests” (see the original German sentence in the next chapter).

Although this is in principle correct, – being deeply impressed by another study of Mendel’s VERSUCHE ÜBER PFLANZEN-HYBRIDEN (1866), – concerning Mendel I think that this comment is unnecessary (as for Galilei and Newton, I do not want to give an opinion here). I presume the proof for the authenticity and precision of Mendel’s work is to be found in – among other things – the paragraph concerning the seventh of the characters studied by Mendel. He writes (p. 11) [English Version according to]:

“With regard to this last character it must be stated that the longer of the two parental stems is usually exceeded by the hybrid, a fact which is possibly only attributable to the greater luxuriance which appears in all parts of plants when stems of very different lengths are crossed. Thus, for instance, in repeated experiments, stems of 1 ft. and 6 ft. in length yielded without exception hybrids which varied in length between 6 ft. and 7 [and] 1/2 ft.”

Thus, in this paragraph Mendel clearly describes a case of heterosis, hybrid vigour, over- or superdominance (as the phenomenon was later named from 1914 [heterosis] onward) (as for the history of the term, the genetical basis of the phenomenon and further examples, see Lönnig 1980:Heterosis bei Pisum sativumL.). Moreover, Mendel describes a second case of heterosis when continuing (pp. 11/12):

“T h e    h y b r i d    s e e d s    in the experiments with seed-coat are often more spotted, and the spots sometimes coalesce into small bluish-violet patches. The spotting also frequently appears even when it is absent as a parental character” (spaced by Mendel).

Without a theoretical basis (which is still controversial for many cases of heterosis even in our age of molecular biology) and in the absence of any experiments, it is not possible to simply ‘invent’ such unexpected phenomena of science. Rather one must “stumble over” such totally unaccustomed and unpredictable curiosities of nature to report them to an amazed audience. Dominance in all of the characters Mendel described was already astonishing enough, but the two cases of overdominance (heterosis, superdominance) represent strong evidence that Mendel had exactly done what he described. (Mendel’s explanation of the superdominant plant length found, “which is possibly only attributable to the greater luxuriance which appears in all parts of plants when stems of very different lengths are crossed” is hardly more than a tautology [here a more inclusive restatement of the phenomenon to be explained: it does not answer the question why the greater luxuriance occurs in all plant parts, of which the unusual plant length is an ingredient]. Mendel’s statement shows that he was really at a loss for any theoretical/genetical answer for the heterosis-phenomenon he had encountered and precisely described.)

One could, perhaps, object that the phenomenon of hybrid vigour had been mentioned before Mendel. However, to describe heterosis for definite characters and organs in definite sizes and quantities in definite species and culture varieties (and all that without any knowledge of the genetical and/or molecular basis of the phenomena reported), so that the experiments not only appear unlikely (in fact, unlikely!), but also prove to be entirely reproducible and true – without really having made them at all – is so improbable that we can confidently forget this objection.

Concerning Mendel’s paper, I agree on the scientific level with Mayr and Stern. Curt Stern stated (1966, p. v): “Gregor Mendel’s short treatise, ‘Experiments on Plant Hybrids’ is one of the triumphs of the human mind. It does not simply announce the discovery of important facts by new methods of observation. Rather, in an act of highest creativity, it presents these facts in a conceptual scheme which gives them general meaning. Mendel’s paper is not solely a historical document. It remains alive as a supreme example of scientific experimentation and profound penetration of data” (Stern and Sherwood 1966). Mayr concurs (1982, p. 726) that by this comment Stern has “so well” characterized Mendel’s achievement.

Double article relating to Nylon eater-bacterium

Two articles in one, with strong scientific details showing  the evolutionary claim to be invalid:

From: ICR

Many supporters of evolutionary theory have claimed that nylon-eating bacteria strongly demonstrate the kind of evolution that can create new cellular structures, new cells, and new organisms.1 However, examining only the apparent, visible beneficial trait can be misleading. Recent research into the genes behind these traits indicates that no evolution has taken place.2 In fact, the genes of nylon-eating bacteria show that they have been degraded through mutation.

The gene that mutated to enable bacteria to metabolize nylon is on a small loop of exchangeable DNA.3 This gene, prior to its mutation, coded for a protein called EII with a special ability to break down small, circularized proteins. Though synthetic, nylon is very protein-like because inventor Wallace Carothers modeled the original fiber based on known protein chemistry. Thus, after the mutation, the new EII protein was able to interact with both circular and straightened-out nylon. This is a clear example of a loss of specification of the original enzyme. It is like damaging the interior of a lock so that more and different keys can now unlock it.

This degeneration of a protein-eating protein required both the specially-shaped protein and the pre-existence of its gene. The degeneration of a gene, even when it provides a new benefit to the bacteria, does not explain the origin of that gene. One cannot build a lock by damaging pre-existing locks. Nylon-eating bacteria actually exemplify microevolution (adaptation), not macroevolution.


  1. Thwaites, W.M. 1985. New Proteins Without God’s Help. Creation/Evolution. 5 (2): 1-3.
  2. Anderson, K.L, and G. Purdom. 2008. A Creationist Perspective of Beneficial Mutations in Bacteria. Proceedings of the Sixth International Conference on Creationism. Pittsburgh PA: Creation Science Fellowship and Dallas, TX: Institute for Creation Research, 73-86.
  3. Yasuhira, K. et al, 2007. 6-Aminohexanoate Oligomer Hydrolases from the Alkalophilic Bacteria Agromyes sp. Strain KY5R and Kocuria sp. Strain KY2. Applied and Environmental Microbiology. 73 (21): 7099-7102.

* Mr. Thomas is Science Writer.


The adaptation of bacteria to feeding on nylon waste


In 1975, Japanese scientists discovered bacteria that could live on the waste products of nylon manufacture as their only source of carbon and nitrogen.1 Two species, Flavobacterium sp. K172 and Pseudomonas sp. NK87, were identified that degrade nylon compounds.

Much research has flowed from this discovery to elucidate the mechanism for the apparently novel ability of these bacteria.2 Three enzymes are involved in Flavobacterium K172: F-EI, F-EII and F-EIII, and two in PseudomonasNK87: P-EI and P-EII. None of these have been found to have any catalytic activity towards naturally occurring amide compounds, suggesting that the enzymes are completely new, not just modified existing enzymes. Indeed no homology has been found with known enzymes. The genes for these enzymes are located on plasmids:3 plasmid pOAD2 in Flavobacterium and on two plasmids, pNAD2 and pNAD6, in Pseudomonas.

Is the evidence consistent with random mutations generating the new genes?

Thwaites claimed that the new enzyme arose through a frame shift mutation. He based this on a research paper published the previous year where this was suggested.5 If this were the case, the production of an enzyme would indeed be a fortuitous result, attributable to ‘pure chance’. However, there are good reasons to doubt the claim that this is an example of random mutations and natural selection generating new enzymes, quite aside from the extreme improbability of such coming about by chance.6

Evidence against the evolutionary explanation includes:

  1. There are five transposable elements on the pOAD2 plasmid. When activated, transposase enzymes coded therein cause genetic recombination. Externally imposed stress such as high temperature, exposure to a poison, or starvation can activate transposases. The presence of the transposases in such numbers on the plasmid suggests that the plasmid is designed to adapt when the bacterium is under stress.
  2. All five transposable elements are identical, with 764 base pairs (bp) each. This comprises over eight percent of the plasmid. How could random mutations produce three new catalytic/degradative genes (coding for EI, EII and EIII) without at least some changes being made to the transposable elements? Negoro speculated that the transposable elements must have been a ‘late addition’ to the plasmids to not have changed. But there is no evidence for this, other than the circular reasoning that supposedly random mutations generated the three enzymes and so they would have changed the transposase genes if they had been in the plasmid all along. Furthermore, the adaptation to nylon digestion does not take very long (see point 5 below), so the addition of the transposable elements afterwards cannot be seriously entertained.
  3. All three types of nylon degrading genes appear on plasmids and only on plasmids. None appear on the main bacterial chromosomes of either Flavobacterium or Pseudomonas. This does not look like some random origin of these genes—the chance of this happening is low. If the genome of Flavobacterium is about two million bp,7 and the pOAD2 plasmid comprises 45,519 bp, and if there were say 5 pOAD2 plasmids per cell (~10% of the total chromosomal DNA), then the chance of getting all three of the genes on the pOAD2 plasmid would be about 0.0015. If we add the probability of the nylon degrading genes of Pseudomonas also only being on plasmids, the probability falls to 2.3 x 10-6. If the enzymes developed in the independent laboratory-controlled adaptation experiments (see point 5, below) also resulted in enzyme activity on plasmids (almost certainly, but not yet determined), then attributing the development of the adaptive enzymes purely to chance mutations becomes even more implausible.
  4. The antisense DNA strand of the four nylon genes investigated in Flavobacterium and Pseudomonas lacks any stop codons.8 This is most remarkable in a total of 1,535 bases. The probability of this happening by chance in all four antisense sequences is about 1 in 1012. Furthermore, the EII gene in Pseudomonas is clearly not phylogenetically related to the EII genes of Flavobacterium, so the lack of stop codons in the antisense strands of all genes cannot be due to any commonality in the genes themselves (or in their ancestry). Also, the wild-type pOAD2 plasmid is not necessary for the normal growth of Flavobacterium, so functionality in the wild-type parent DNA sequences would appear not to be a factor in keeping the reading frames open in the genes themselves, let alone the antisense strands.Some statements by Yomo et al., express their consternation:

    ‘These results imply that there may be some unknown mechanism behind the evolution of these genes for nylon oligomer-degrading enzymes.

    ‘The presence of a long NSF (non-stop frame) in the antisense strand seems to be a rare case, but it may be due to the unusual characteristics of the genes or plasmids for nylon oligomer degradation.

    ‘Accordingly, the actual existence of these NSFs leads us to speculate that some special mechanism exists in the regions of these genes.’

    It looks like recombination of codons (base pair triplets), not single base pairs, has occurred between the start and stop codons for each sequence. This would be about the simplest way that the antisense strand could be protected from stop codon generation. The mechanism for such a recombination is unknown, but it is highly likely that the transposase genes are involved.

    Interestingly, Yomo et al. also show that it is highly unlikely that any of these genes arose through a frame shift mutation, because such mutations (forward or reverse) would have generated lots of stop codons. This nullifies the claim of Thwaites that a functional gene arose from a purely random process (an accident).

  5. The Japanese researchers demonstrated that nylon degrading ability can be obtained de novo in laboratory cultures of Pseudomonas aeruginosa [strain] POA, which initially had no enzymes capable of degrading nylon oligomers.9 This was achieved in a mere nine days! The rapidity of this adaptation suggests a special mechanism for such adaptation, not something as haphazard as random mutations and selection.
  6. The researchers have not been able to ascertain any putative ancestral gene to the nylon-degrading genes. They represent a new gene family. This seems to rule out gene duplications as a source of the raw material for the new genes.8

P. aeruginosa is renowned for its ability to adapt to unusual food sources—such as toluene, naphthalene, camphor, salicylates and alkanes. These abilities reside on plasmids known as TOL, NAH, CAM, SAL and OCT respectively.2 Significantly, they do not reside on the chromosome (many examples of antibiotic resistance also reside on plasmids).

The chromosome of P. aeruginosa has 6.3 million base pairs, which makes it one of the largest bacterial genomes sequenced. Being a large genome means that only a relatively low mutation rate can be tolerated within the actual chromosome, otherwise error catastrophe would result. There is no way that normal mutations in the chromosome could generate a new enzyme in nine days and hypermutation of the chromosome itself would result in non-viable bacteria. Plasmids seem to be adaptive elements designed to make bacteria capable of adaptation to new situations while maintaining the integrity of the main chromosome.

Stasis in bacteria

P. aeruginosa was first named by Schroeter in 1872.10 It still has the same features that identify it as such. So, in spite of being so ubiquitous, so prolific and so rapidly adaptable, this bacterium has not evolved into a different type of bacterium. Note that the number of bacterial generations possible in over 130 years is huge—equivalent to tens of millions of years of human generations, encompassing the origin of the putative common ancestor of ape and man, according to the evolutionary story, indeed perhaps even all primates. And yet the bacterium shows no evidence of directional change—stasis rules, not progressive evolution. This alone should cast doubt on the evolutionary paradigm. Flavobacterium was first named in 1889 and it likewise still has the same characteristics as originally described.

It seems clear that plasmids are designed features of bacteria that enable adaptation to new food sources or the degradation of toxins. The details of just how they do this remains to be elucidated. The results so far clearly suggest that these adaptations did not come about by chance mutations, but by some designed mechanism. This mechanism might be analogous to the way that vertebrates rapidly generate novel effective antibodies with hypermutation in B-cell maturation, which does not lend credibility to the grand scheme of neo-Darwinian evolution.11


  1. Kinoshita, S., Kageyama, S., Iba, K., Yamada, Y. and Okada, H., Utilization of a cyclic dimer and linear oligomers of ε-aminocapronoic acid by Achromobacter guttatus K172, Agric. Biol. Chem. 39(6):1219–1223, 1975. Note: A. guttatus K172 syn. Flavobacterium sp. K172. Return to text.
  2. Negoro, S., Biodegradation of nylon oligomers [review]Applied Microbiology and Biotechnology 54:461–466, 2000. Return to text.
  3. A plasmid is an extra-chromosomal loop of DNA in a bacterium. Such loops of DNA, unlike the chromosomal DNA, can be swapped between different species of bacteria. An individual bacterium can have several types of plasmid, and multiple copies of each. Return to text.
  4. Thwaites, W.M., New proteins without God’s help, Creation/Evolution 5(2):1–3 (issue XVI), 1985. Return to text.
  5. Ohno, S., Birth of a unique enzyme from an alternative reading frame of the preexisted, internally repetitious coding sequenceProceedings of the National Academy of Sciences USA 81:2421–2425, 1984. Return to text.
  6. Truman, R.Protein mutational context dependence: a challenge to neo-Darwinism theory: part 1Journal of Creation 17(1):117–127; Truman, R. and Heisig, M., Protein families: chance or design? Journal of Creation 15(3):115–127. Return to text.
  7. As of the date of writing, no Flavobacterium sp. genome has been sequenced. Return to text.
  8. Yomo, T., Urabe, I. and Okada, H., No stop codons in the antisense strands of the genes for nylon oligomer degradationProceedings of the National Academy of Sciences USA 89:3780–3784, 1992. Return to text.
  9. Prijambada, I.D., Negoro, S., Yomo, T. and Urabe, I., Emergence of nylon oligomer degradation enzymes in Pseudomonas aeruginosa PAO through experimental evolutionApplied and Environmental Microbiology 61(5):2020–2022, 1995. Return to text.
  10. Bacterial Nomenclature Up-to-date, Deutsche Sammlung von Mikroorganismen und Zellkulturen GmbH, Braunschweig, Germany. <>, 18 September 2003. Return to text.
  11. Truman, R.The unsuitability of B-cell maturation as an analogy for neo-Darwinian Theory, March 2002; <>, 22 August 2003. Return to text.

God bless you very much!

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