Evidence of Stasis

Mismatch Repair (MMR)

A new discovery by biochemists Paul Modrich PhD, and others at Duke University Medical Center, shows that the mismatch repair system senses certain types of DNA damage, which leads to activation of the cell's suicide machinery, called apoptosis, resulting in cell death. If the MMR operating system fails, it can result in development of several types of cancer including malignant tumors on the inner wall of the large intestine. MMR after discovering errors in DNA replication repairs the mistaken nucleotide combinations so that the adenine is paired with a thymine and the guanine with a cytosine - both pair situated on the double-strand DNA molecule. Thus the MMR mechanism guards cells against mutations by rectifying mistakes occurring during chromosome replication.

"Mutations, by nature of being mutations, violate the "Watson-Crick" pairing rules by creating unpaired bases within the helix due to the presence of the unique mutation or the erroneous duplicate. Normally, however, the "cellular mismatch repair system" recognizes these mismatches, identifies the hopeful usurpers, and eliminates them from each and every strand of DNA" (Modrich 1994).

"Although these mechanisms cannot drive the mutation rate to zero, they are finely tuned to minimize it." (Haynes, 1988: 577-584)

It is clear that DNA repair enzymes and other repair systems have a role in maintaining stasis.

Post translation modification

In this process the raw proteins are cut to size or biochemically modified by cells. The most frequent 'post translational modification' is the so-called N-linked bonding of proteins with sugar building blocks but hundreds of other modifications exist and each have an important role in regulating the expression of huge numbers of proteins during ones lifetime.

Some of the post translation modifications are:

proteolysis - often involves the removal of initiator methionine or of signal sequences needed to help membrane proteins locate within the appropriate membrane

glycosylation - essential for proteins, especially membrane proteins, involved in the immune system and involves the addition of complex carbohydrates to amide or hydroxyl groups found on the protein.

phosphorylation - the process of adding phosphate groups to hydroxyl groups in serine, threonine and tyrosine residues in proteins particularly those involved in signalling pathways. The process is usually reversible and the exchange of phosphates is a crucial part of the signalling process.

acylation - by either acetyl or myristoyl groups often occurs on the N-terminal end of the protein following removal of the initiator methionine.

Almost all proteins undergo post translational modification which for example, influence mRNA stability, translational efficiency, protein turnover rate and transcription factor structure. All this happens as the organism responds to environmental stimuli. Post translation modification is the last step in conveying genetic information from a gene to a functional gene product. Improper functioning of post translational modification especially glycosylation cause different autoimmune syndromes.

Therefore, post translational modifications are another way by which stasis is maintained. They function as varieties of protein degradation that recognize and eliminate abnormal proteins. For new type of organism to develop there is a need for new proteins however the biochemical reactions above counteract any change.

Nuclear cytoplasmic stasis

There is strong evidence that there are cytoplasmic regulatory molecules that decode DNA. These regulatory molecules together with the DNA prevent change and inhibit the already slow Darwinian evolution process. This was proven experimentally by nucleus transplantation, removing the nucleus from one cell, and replacing it with the nucleus from another cell.

When the nucleus from the egg of the frog Xenopus laevis laevis was removed and replaced with the nucleus from the embryo of Xenopus tropicalis the egg never developed beyond the neurula stage, or the stage when the primitive band is first developed. However when the egg of the Xenopus laevis laevis united with the nucleus from an embryo of Xenopus laevis laevis a fully adult frog developed. (Gurdon 1962)

A similar experiment was performed with the protozaoans Amoeba proteus and Amoeba discoides. When the nucleus from A. discoides was transplanted into the enucleated cell of A. proteus, only 1% of the cells survived. This natural phenomenon is known in the scientific circles as transplantation incompatibility.

The explanation for this is that the regulatory molecules in the cytoplasm of B species, fromwhich the nucleus was removed, could not decode the foreign DNA upon receiving the nucleus of A species.

Another explanation for the incompatibilities is that, the eggs of one species have a protective covering (called the zona pellucida ) which prevents the entry of sperm of another species. The protective covering is covered with "locks" which open only to one kind of "key," carried by the sperm of the same species. If a sperm's key does not fit into the egg's lock, the egg will not let it in. In rare cases, two closely related species may have "sperm keys" and "egg locks" that are so similar that the sperm key of one sometimes manages to fit into the egg lock of the other, and cross-species fertilization occurs. (E.g. horse and donkey resulting in a mule a sterile or infertile hybrid.)

J.M. Barry (1986) conclusion remains valid:

"The possibility is often overlooked that each generation of organisms must inherit not only DNA from the previous generation but also other cell components peculiar to that species. All in all, it seems that there are strong objections to the development of macromutations. If the egg develops a mutation, still it is very unlikely that at the same time another mutation would produce the exactly right regulatory molecules to express the new characteristics of the egg. Conclusively, if these mutations do not occur at same time, there will be no chance for the prosperous development of the embryo."

The opposing opinion is that as a new species is evolving, due to DNA mutation, new structures in the cell components also develop to ensure survival of the new mutations in DNA.

However, beneficial mutations are extremely rare what this means is that the creation many varieties of forms and functions is extremely unlikely. We will give a few interesting examples and conclusions about beneficial mutations. This topic will be explained in more detail in another article.

The opposing opinion is that as a new species is evolving, due to DNA mutation, new structures in the cell components also develop to ensure survival of the new mutations in DNA.

Examining this hypothesis by way of an example, humans have approximately 3 billion DNA base pairs this means that 2% of that is around 60 million DNA base pairs. If we were, for the sake of argument to accept, as new research suggests, that the humans separated from a common ancestor 5.4 million years ago The implied rate of new mutations is 2.4 to 4.8 per individual. This is without considering the mutations lost owing to genetic drift, the lethal mutations or mutations that occur in DNA that do not code for protein.

Interestingly, in 1999 Geneticists Adam Eyre-Walker, from the University of Sussex in Brighton, and Peter Keightley, from the University of Edinburgh carried out a research in which they calculated the rate at which human genes have mutated since our ancestors split from chimpanzees six million years ago. Keightley said: "We estimate that about 4.2 new mutations have occurred on average every generation in the human lineage since we diverged from the chimpanzees, and that 1.6 of those are deleterious."

Both of them calculated the time of divergence to be 6 million years ago. But even if we accept the new information that the chimps and human diverged 5.4 million years ago still the accumulation of deleterious mutations v. 'beneficial' is so high that without other factors intervening the human race should be extinct by now.

In our view whether evolution can occur or not, the extreme rarity of beneficial mutations should be seriously considered. What this means is that the creation of many varieties of forms and functions is extremely unlikely. This is because beneficial mutations or rare beneficial units completely disappear when we analyze mutations as they occur, within clusters which are physically linked and inherited as if a single trait. Any linked mutation cluster will be inherited as a single genetic unit, and the effect of that mutation cluster will simply be the net effect of all of its component mutations. The fitness effect of any cluster can be calculated to be the average effect of its individual mutations times the number of mutations within that cluster. It is highly probable that any rare beneficial mutation will be quickly cancelled out. Since the vast majority of mutations are deleterious, each mutation cluster will have an increasingly negative affect on the fitness of each generation. In the time taken for two mutations per linkage group, nearly all beneficial mutations will have been cancelled out by at least one linked deleterious mutation. As the mutations accumulate beyond two mutations per cluster, it becomes increasingly certain that there will be no linked cluster left with a net beneficial effect. (J. Stanford)

Another example is penicillin resistance in bacteria to, aureomycin and chloromycetin. It was believed that the resistance occurred as a result of beneficial mutations due to the influence of the antibiotics. However, this was discovered to be incorrect when it was found that mutations spontaneously occur in bacteria without exposure to antibiotics.

Following many similar observations, the theory of the hopeful monster was developed in the early1980's. This advocates a sudden mutations every 50, 000 years producing a new species all at once. This topic will be discussed later.

Following experiments on 10,000 generations of E-coli bacteria the conclusions were: Since there is no selective pressure, new mutations are rarely beneficial and thus they fade within the population. The experimental populations were large so that the same mutations could occur, but with different sequences of mutation for each population. Consequently, some populations incorporated mutations that were beneficial over the short-term but longer term led to evolutionary dead ends.

Populational stasis

A new mutation could become permanent only if it is beneficial and successfully avoids the DNA repair system and does not interfere with cytoplasmic regulatory mechanisms. Even if the mutation avoids the cellular mechanism of stasis, and even if, being beneficial, it spreads in the population, great transformations do not occur due to microevolution. This microevolution helps the species to exist under different environmental conditions. One well known example we gave was industrial melanism but this and many other examples only prove that microevolutionary development does not change the basic species but only helps the organism to adapt to environmental change. We conclude that microevolution helps to maintain stasis rather than enhance development toward macroevolution or changing the organism from one species into another. It can be argued that many small changes accumulated over millions of years result in macroevolutionary change. Although this appears a strong argument, there is no observational evidence and the fossil record supports the idea that there is only macroevolutional change in the species. We will deal further with the fossil records elsewhere. Michel Cremo in his books "The Forbidden Archeology" or its smaller version "The Hidden History of Human Race" gives many examples of stasis.

Returning to the example of E-coli's novel metabolic capabilities, Barry Hall (1983) observed, that they did not change the E-coli into another type of bacteria. This kind of small change is ascribed to microevolution and therefore favorable to maintaining stasis. The small biochemical changes said to be 'evolution' of the bacteria actually preserve the bacteria type. Transformations to non-bacterial characteristics were never observed. This was confirmed by Zubay (1988: 957) with his experiments on bacteria affected by the antibiotic streptomycin, which is supposed to cause lethal disruption of protein synthesis. Some bacteria developed mutations in the genes for their ribosomal proteins that allowed their ribosomes to function unhindered by streptomycin. The mutated ribisomes were still typically bacterial.

Some evolutionists say that the terms microevolution and macroevolution are not found in biology, they are just invention. However, other evolutionists accept that variations within a gene pool, based on the pool's existing genetic mix is actually microevolution. M. Denton in his book Evolution: A Theory in Crisis, on page 83 says: "If we want absolutely bona fide evidence for the reality of microevolutionary change and speciation in nature, the cases of the circumpolar overlaps and the fruit fly of Hawaii come very close ..."

Some other examples of microevolution that obviously maintained the species (stasis) by helping them to adopt to new environments are:

1. unique but related species of Hawaiian fruit flies on various islands;

2. unique but related species finches in Galapagos Islands;

3. unique but related species of tortoises in Galapagos Islands;

4. finch beaks ("evolution in action");

5. industrial melanism;

6. English sparrows in USA;

7. artificial selection (dog breeding);

8. Madeira rabbits;

9. In humans, skin colour, mongoloid eye, short stout eskimos, tall thin Africans

In conclusion, in this essay we have mentioned testable mechanisms of stasis that are known to scientists. They work at many different levels enabling the steady maintenance of the species. It is time to examine them seriously, without scientific and philosophical prejudice.

For further discussion of minor changes or microevolution that we could call microdevolution owing to genetic degeneration, please read the essay "Cyclical creation & Devolution".