Benaficial Mutations And Evolution

The Nylon Bacteria

Another example for evolutionists are the two bacteria: Flavobacterium sp. K172 and Pseudomonas sp. NK87. These two bacteria, discovered around 1975 have the ability to hydrolyse nylon oligomers. This is 40 years after the invention of nylon by Wallace H. Carothers in 1935. Although these bacteria are popularly known as 'nylon bugs', they do not eat nylon. What they digest are the nylon oligomers: E-caprolkctum, 6aminohexanoic acid, 6-aminohexanoic acid cyclic dimmer; and 6-aminohexanoic acid oligomers that are water-soluble chemicals associated with the manufacture of nylon, found in the waste water of nylon factories.

Initially, it was thought that these new types of nylon oligomer digesting bacteria were the result of an existing gene duplication followed by a "frame shift" mutation. Scientists arrived at this conclusion by comparing the genome of the "nylon bug" to the genome of their non-nylon eating ancestors. The frame shift mutation occurred by insertions of T (thymine) that changed the codons, a sequence of three successive nucleotides in nucleic acid.

NOTE: A codon is a triplet or a combination of three nucleotides found in the genetic material of DNA - adenine (A), cytosine (C), guanine (G), and thymine (T); and RNA- adenine (A), cytosine (C), guanine (G), and uracil (U).

The result of this frame shift mutation meant the bacteria got an ability to break down the nylon oligomer from nylon waste and obtain energy from that source.

The bacteria do not get much energy from breaking down the nylon waste and far from being able to digesting nylon. However, they get sufficient energy for survival by the new food source, enabling the bacteria to live in a new environment. The newly developed enzymes are very inefficient and possess only 2% of productivity of normal enzymes. As a result of the changes Flavobacterium sp.K172 can no longer metabolize carbohydrates Cn(H2O)n, their bacterium's original food.

The scientists hope that future mutations will increase the efficiency of the process. These mutations would allow the bacteria to develop into bacteria that live solely on nylon and other man made fibres making them biodegradable.

The New Evidence

Yomo et al, 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 many stop codons.

NOTE: Codons are the three triplets (UAA, UAG, UGA) which terminate protein synthesis.

New evidence shows that the ability of the bacteria to digest nylonase was due to plasmids. [K. Kato, et al., 'A plasmid encoding enzymes for nylon oligomer degradation: Nucleotide sequence analysis of pOAD2', Microbiology (Reading) 141(10):2585-2590, 1995.] The Encyclopedia Britannica describes the plasmids in the following way: Plasmids are circular deoxyribonucleic acid (DNA) molecules that replicate independently of the bacterial chromosome. They are not essential for the bacterium but may confer a selective advantage. One class of plasmids, colicinogenic (or Col ) factors, determines the production of proteins called colicins, which have antibiotic activity and can kill other bacteria. Another class of plasmids, R factors, confers upon bacteria resistance to antibiotics. Some Col factors and R factors can transfer themselves from one cell to another and thus are capable of spreading rapidly through a bacterial population. A plasmid that is attached to the cell membrane or integrated into the bacterial chromosome is called an episome (q.v.)".

Briefly, the plasmids are:

" Transferred during conjugation

" Carry genes for inactivation of antibodies, toxins

" Serve as a rapid means of transmission of genetic information in a rapidly changing environment

What happened in this case is that the bacterial plasmids enabled adaptation to a new food sourc,e the nylon oligomer. Susumu Ohno from the 'Beckman Research Institute of The City of Hope' describes this in the following way:

"When pOAD2 plasmids encountered nylon by-products, an insertion of T [Thymine]…proved advantageous, for this insertion silenced the PR.C. coding sequence by creating the T-G-A chain terminator; at the same time, the newly emerged A-T-G created a new coding sequence from an alternative open reading frame, which happened to specify a polypeptide chain with 6-AHA LOH activity for degradation of nylon byproducts."

The Flavobacterium Sp. K172, that was formerly known as Acromobacter guttatus Sp. K172 (2), has acquired two plasmid-encoded enzymes for sequential degradation of nylon oligomers. The two enzymes responsible for metabolism of 6-aminohexanoic cyclic dimer are technically, the 6-aminohexanoic acid cyclic dimer hydrolase (6-AHA CDH) and 6-AHA LOH (2, 3)". Susumu Ohno is remarking that the swiftness with which these two enzymes have evolved is remarkable, because several decades for their development is nothing in the evolutionary time scale.

Does is this example of nylon oligomer digesting bacteria a proof of evolution? Certainly, the argument that the bacteria are still only bacteria is one of the statements that the evolutionists do not like to accept but it is still fact. An example of microevolution, cannot prove macroevolution or a change on the morphological level. The mutation did not have any effect on morphology of the bacteria. Some bacteria existing now are very similar, indeed almost indistinguishable from the bacteria of 3.5 billion years ago. The recent beneficial mutation that caused the development of a nylon bug did not create a different type of bacterial population but a sub-population that can exploit a new environment. We can see that the same thing happened with the finches studied by Darwin, and canines, that now have hundreds of subpopulations. Because bacteria developed the ability to degrade nylon does not mean that they are not bacteria but something else. What is surprising is that the mutated Flavobacterium sp.K172 was better in digesting its previous food than the nylon oligomers and the changes have left it unable to metabolize carbohydrates. Thus, the natural question that arises is this evolution if we take the consideration of the definition of evolution that is - 'development of the species to a more advanced or mature stage'? To consider a small-scale adaptation to be an evolution is wishful thinking.

Sickle Cell Trait

Resistance to malaria by having SCT (sickle cell trait) is used by evolutionists as a proof of evolution. There are some serious problems with this idea. It is estimated that world wide approximately 250 million people suffer from malaria and around 2.5 million die each year. Years of observation have that SCT cannot give full protection to people from malaria. This is not all. Carriers of SCT pay a price for this. Some have occasional painful episodes, especially when flying, some have blood in their urine. The trait is also hereditary and children and adults get sickle cell anemia. When both parents are SCT carriers, there is a 25% chance that their child will die from sickle-cell anemia, and another 25% chance that that the child will have normal hemoglobin, but die from malaria in areas where malaria is endemic.

There is no doubt that the carriers of SCT are better able to survive in malaria endemic areas but, their defective hemoglobin has poorer function than a person without SCT. According to JA Kark, DM Posey, HR Schumacher, and CJ Ruehle (1978) SCT or hemoglobin AS carriers have increased risk of sudden death during physical training. Similar research in 2001, on three sudden death cases due to physical exertion, confirmed that sickle cell trait is a potentially fatal disorder. The report from the University of Texas-Southwestern Medical Center, Department of Pathology, Dallas, USA states: "In all three cases, postmortem hemoglobin electrophoresis demonstrated hemoglobin AS. In none of the cases was the body temperature found to be elevated. These cases serve to remind the forensic community that, in the proper setting, sickle-cell trait must be viewed as a potentially fatal disorder".

What exactly happens is that sickle cell anemia results from the replacement of one amino acid for another amino acid on each of the two beta chains of hemoglobin. Because of this amino acid switch in hemoglobin, the molecule changes shape. The changed hemoglobin molecules cause a change of the shape of red blood cells that can result in their inability to pass through some small blood vessels. This might result in death, especially where these tissues are in the brain.

Statistically, the more carriers of SCT are there in a population, more people will be born with sickle cell anemia. It is important to recognise that SCT is detrimental to leading a normal life. In central Africa, for example, SCT is associated with a higher prevalence of multiple infections.

It is surprising how evolutionists can mention SCT as an advantageous development as there are so many obvious problems caused by this mutation. Though this mutation helps one problem, malaria, it causes many others. Thus, we cannot accept this example as positive proof of evolution. It is, again a change at the genetic level and not morphological. Microevolution and not macroevolution, change within the species and not change into another species.