Benaficial Mutations And Evolution

Benaficial Mutations And Evolution

Definitions

According to science mutations are relatively permanent changes in DNA or the gene sequence caused e.g. by environmental influences like radiation, mutagenic chemicals or random events. Some mutations will cause abnormal function and some mutations have no effect. However, if these were the only two types of mutations to exist life on earth would become extinct. There is a third type of mutation called a beneficial mutation. When many beneficial mutations accumulate, a new species may develop. Whether this last is correct is open to question. Below we examine the questions that may be asked.

The first question is 'are beneficial mutations necessary?' For example, when there are environmental changes, a beneficial mutation (BM) can have a role helping an organism to adapt to changed circumstances. But, beneficial mutations (BMs) also occur when no environment change takes place. Why is this? Since many mutations are harmful and some of these will become fixed in the genome, other mutations are required to eliminate the potential harm so that the organism can survive. Thus, these compensatory and back mutations are considered beneficial. It follows therefore in a stable environment very few if any mutations will be truly beneficial.

A back mutation is defined as a mutation that reverses a previous mutation. As mutation and back mutation rates are slow it takes a long time to reach an equilibrium

Additive mutations are frequently back-mutations at loci that have undergone fixation, whereas compensatory epistatic mutations involve alleles at other loci.

If we consider the most common examples of BMs and analyze them, do they provide proof for evolution?

Examples

Antibiotic resistance in bacteria

According to the modern evolutionary theory, a mutation is defined as a change in the sequence of the base pairs in a DNA molecule. It can supply new genetic mechanisms for genetic activity and thus mutation explains the action of evolution in and the common descent with modification.

Microorganisms such as bacteria that undergo beneficial mutations and gain antibiotic resistance is the most often mentioned example of evolution in action. Theoretically, mutations in the bacteria that give resistance to antibiotics and thus ensure survival are beneficial. Thus natural selection will give rise to a bacteria better adapted to the new environment.

The history of fighting disease shows that bacteria are very good at rapidly developing resistance to antibiotics. This means that there is a constant battle to develop more effective antibiotics. There are two considerations:

1. Most of the mutations bacteria undergo are caused by antibiotics. The different types of mutations can harm some cellular functions of the bacteria but after the antibiotic attack is over the bacteria undergoes a permanent change.

2. Secondary mutations restore the primary fitness of the bacteria.

So, an evolutionist would say these mutations are BMs because they enhance evolutionary development. However, do mutations in bacteria cause evolution or is there evolution in morphological sense? To examine this it is worth looking at a short analysis of mutations at the molecular level.

The following list examines some bacteria and the mutations they undergo to ensure survival in the new antibiotic affected environment.

Rifampin resistance: arises due to a point mutation of a subunit of RNA polymerase. In the laboratory high levels of rifampin resistance can be attained by eliminating the binding affinity of RNA polymerase to rifampin.

Fluoroquinolones resistance: the antibiotic targets the DNA gyrase of bacteria consisting of gyrA and gyrB. Point mutation in either of these two genes results in antibiotic resistance. (These two examples although "beneficial" by nature, do not give a useful model of the origin of antibacterial resistance or i.e. the origin of the gyrase's affinity for the fluoroquinolones.)

Streptomycin resistance: occurs due to a mutation in the 16S rRNA gene, that greatly reduces the affinity of streptomycin for the 16S molecule. The oligopeptide's reduction of transportation activity can also result in resistance to some other antibiotics. In these examples, resistance occurred because of the loss of a functional component/activity.

Metronidazole resistance: - comes about in several ways, a) When by a missense mutation (a single amino acid change), the activity of the NADPH nitroreductase is seriously reduced, b) by nonsense or deletion mutations in rdxA the reductase activity is lost - the metronidazole no longer activated. These mutations cause a loss of the enzyme activity necessary drug effectiveness in the cell. Loss of enzymatic activity does not describe how the enzyme originally "evolved" and thus, it cannot be a true example of evolution.

Initially, it was believed that bacteria would be unable fight multiple antibiotics because they could not evolve resistance in the complex environments that the multiple antibiotics create. However, this proved to be untrue for all cases. Some bacteria, like E coli solve this problem by producing a multiple-antibiotic-resistance (MAR) efflux pump (made by MarA and MarB proteins) This ejects the antibiotics from the cytoplasm of the cell where the concentration is below the lethal level. Moreover, if a mutation removes the suppressing control of MarR (a regulatory protein of MarA and MarB) this results in overproduction of MarAB efflux pump that can cope with very high concentrations of antibiotics.

Alekshun and Levy (1999), discovered that the MarA protein can also act as a regulatory agent increasing the production of MarA and MarB proteins. Thus, if there is increased activity of MarA, this increases the ability to expel antibiotics from the cell and keep them out of the cell. Although, in this case the mutation enhances the production of efflux pump that helps the bacteria to reject antibiotics, as we see, the mutation although beneficial, also causes a loss of regulatory control, the repressor protein, MarR. There is no genetic mechanism to explain the origin of this regulatory control.

Erythromycin resistance: this results from the loss of the 11 base pair segment of the 23S rRNA gene or a mutation that modifies the verification of the 23S rRNA, reducing the affinity of the ribosome for the antibiotic.

Chloramphenicol resistance: is a result of the removal of the peptidyltransferase gene's 12 base pair region in domain II.

Cephalosporin resistance: occurs through modification of the membrane transport kinetics.

Actinonin resistance: depends on a mutation that removes the fmt gene expression in Staphylococcus aureus.

Zwittremicin resistance: as observed in E-coli is due to loss of proton motive force.

Penicillin tolerance: in Streptococcus gordonii this is a result of a loss regulatory control of the arc operon

Resistance to ß-lactams: - like ampicillin, is caused by preventing cell division. This makes the cell of the E-coli less sensitive to the lethal effect of the antibiotic.

As can be seen, all these examples of antibiotic resistance are a result of a mutation that causes the loss of a biological system, including cell division and proton motive force and thus, although beneficial for survival of the bacteria, they are examples rather of devolution, than evolution. Obviously, proof of evolution and the predictions of "descent with modification" is not provided by these examples. But looking at further examples:

Kanamycin resistance: results from a loss or diminution of Oppa, a transport protein.

Ciprofloxacin, imipenem, meropenem and cefepime resistance: occurs due to decreased formation of the outer membrane porin, Ompf.

We could give more, similar examples but the conclusion would be the same: antibiotic resistance mutations with reduction or loss of regulatory and transport systems cannot provide the required genetic mechanism for evolution or common descent. It is rather an example of loss or reduction of cellular function that is contrary to predictions of evolutionary theory. Therefore in conclusion these mutations cannot provide a mechanism that can increase the protein activity required for normal cellular function. They are not examples of evolution due to beneficial mutation or a special development. Saunders (1984) showed that antibiotic resistant bacteria existed before antibiotics developed.

In this analysis, whilst these mutations are beneficial and help the bacteria to become resistant to antibiotics, such gains have a price. First, the ability to survive is decreased in an antibiotic free environment. This causes slow growth rates and slow protein synthesis. When the antibiotic danger for the bacteria is over they can undergo a further beneficial mutation, and restore fitness of the normal cellular function etc. This was demonstrated in novel laboratory circumstances that resulted in the appearance of BMs in bacteria and yeast. (Paquin et al, 1983; Lenski et al, 1991)

Minnich in his repeatable, laboratory experiments on the evolution of antibiotic resistance in bacteria showed that when returned to a pool of non-resistant bacteria where the antibiotic is not present, the resistant bacteria are killed quickly by the bacteria that lack resistance. Thus, adaptation of resistance comes at the price of overall fitness. This suggests that there are limits to how far bacteria can evolve and remain viable in a natural setting. This is evidence that contradicts Darwinism. However, the University of Idaho has prohibited Scott Minnich from mentioning this to his students. These laboratory results, repeatable by any sufficiently equipped laboratory, are deemed unacceptable. Was this the University of Idaho's intention? Can the University justify this stance of rejecting laboratory evidence that runs contrary to modern evolutionary theory?

However, are these beneficial mutations in bacteria really a step toward large morphological changes or in the evolution of bacteria to some other species? Patently this is not so. The bacteria is basically the same bacteria and not something else. "Nature" (8.6.2000) reported the discovery of a sulphur deposit containing fossil micro-organisms. Birger Rasmussen, from the University of Western Australia, estimated the age of these fossils to be 3,235 million years. This is the oldest bacteria like fossil found. Evolution theory assumes that living entities like bacteria undergo substantial change over time, eventually developing into multi-celled organisms. However, there are some serious objections and challenges. Fossils from the 'Cambrian explosion' fail to support this hypothesis and there is also the question of how can the theory of evolution explain a bacteria 3,235 million years old, similar to those living nowadays, already had a complicated cell structure. Since this bacteria belongs to the prokaryotes (literally, "before the nucleus"), what evidence if there for its existence before the evolution of cells with a nucleus. That these oldest bacteria had a common ancestor is not clear.

This is a topic to be discussed in more detail in another essay.