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Evolution: the Devil is in the Details (part Three of Four)
Two Types of Mutations
Are mutations the driving force in evolution? Is that feasible? Let's check it out.
Considering all the activity in the cell - and we have only looked at a small part of it - it appears that a good number of things could go wrong in the operation. That is an understatement. Geneticists call these errors: saltations, mutations, mutants, sports, or "freaks". Those who write or speak on evolution usually refer to them as mutations. We find two basis types: gene and chromosome mutations.
Gene mutations occur when nucleotide sequences are altered in the DNA helix. One nucleotide base is substituted for another, or perhaps a base is added or deleted. What happens?
Let's say one nucleotide is substituted for another. That's the most common gene accident. If the first adenine (A) molecule of a GAA codon were to mutate into a uracil (U), it becomes a GUA codon. The upshot of this change is that we now have a sequence coding for a valine amino acid instead of a glutamic acid.
This simple, one nucleotide base substitution causes sickle cell anemia. Distorted sickle cells get stuck in tiny blood vessels preventing blood cells from carrying oxygen into the body.
That is so remarkable, it bears repeating. If just one microscopic nucleotide out of three billion goes astray, you could die. That example is not unique. Other nucleotide changes result in consequences varying from negligible to lethal.
Gene mutations are nucleotide accidents. Sometimes a nucleotide is missing or one is repeated or duplicated. That can throw the whole gene out of kilter. A single missing nucleotide can result in a missing protein. If the protein remains, it is likely to be a huge malfunctioning entity. Deformity or death is the most likely prospect for any individual with one or more deleted nucleotide bases. Adding or duplicating a nucleotide in the DNA sequence would reek equal havoc.
A deletion of one or more nucleotides is the gene mutation equivalent of removing the back of your watch and unscrewing one or more of the tiny screws inside of the watch. Would this "screw deletion" likely improve the watch's performance, or harm it? Or would you be surprised if the watch ran at all?
An addition of one or more nucleotides is the gene equivalent of removing the back of your watch and jamming in one or more extra tiny screws. Would that help, hurt, or destroy the watch? And a substitution of one or more nucleotides is the gene mutation equivalent of removing the back of your watch and replacing one or more screws with screws of a different size or even something other than a screw. Once more, it's a pretty sure bet that the change will be detrimental for the watch.
A DNA mutation is nothing more than a mistake, an error jammed into the DNA sequence. Any tampering with what makes a living thing tick is likely to kill or maim it. Occasionally, a gene mutation is neutral. Rarely is it beneficial. Seventeen years of fruit flies prove it. (We will address both beneficial mutations and the fruit fly experiment in future articles.)
In addition to gene mutations, we also find chromosomes mutations. We know that a gene is nothing more than a section of DNA which codes for one or more traits - color of eyes, skin, hair, or length or shape of the nose, ears, etc.
Often a single human characteristic depends upon a combination of several genes. You and I have about 100,000 genes in our bodies. They are organized into 46 chromosomes. Looking at it from the top down, we can say, chromosomes are collections of genes which in turn are collections of DNA sequences.
Chromosomes come in pairs. Normally the male and female each contribute one member to each pair. The number, size, and organization of chromosomes vary among species. At the low end of the totem pole, bacteria have only one chromosome. At the high end of the spectrum, many species have more chromosome than we do. Butterflies have more than 100 pairs, while ferns show more than 600.
Changes in the number, size, or organization of chromosomes are called chromosome mutations. Two chromosomes may fuse into one; or one breaks into two; or a chromosome duplicates itself or is deleted. On rare occasions, the whole chromosome rotates 180 degrees at the same location.
Then again, one or more genes will break off one chromosome and join another. Geneticists call this rearrangement "crossing over." A pair of chromosomes exchange a section of one or more genes. Linkage between the genes suddenly and dramatically changes.
Traits which were once closely linked become separated and vice versa. Physical traits are seen in new combinations with greater variety. Sure, variety is the spice of life. But how does this type of mutation fit into evolution? It doesn't. A mishap at the chromosome level does not crank out new traits. It merely reshuffles old ones. We cannot go from bacteria to humans by scrambling chromosomes. It is just another dead end for macroevolution.
Our brief look at mutations really hasn't cleared anything up. Naturalists, you may remember, say that mutations are the driving force behind evolution. Of course, natural selection lops off the rough edges, but mutation is the spark plug - the creative source for engineering new species.
But when we look at the two types of mutations, neither seems promising. Gene mutations produce diseases, monsters, or death, with an occasional neutral result. It is suggested that perhaps on extremely rare occasions, something beneficial might occur. That doesn't seem too encouraging for the bacteria to man scenario.
Even less promising are chromosome mutations which merely mix already existing characteristics. So what makes evolution tick?
Mutations: Facts and Figures
Let's start off where naturalists usually begin - with something like a bacteria. Never mind how those three million nucleotides got together and organized into a living system. Let's just say the bacteria-like life form is a given.
How is the bacteria suppose to change? Answer: by mutation. Immediately we run into a problem. Mutations are very rare. Even more discouraging, the simpler the organism, the fewer the mutations. And nothing alive is more simple than a one-celled bacteria type of organism.
On the average, one mutation would show up in every 500,000 of these creatures. That's a slow start. But coming up with a mutation is only the first of many hurdles. The second hurdle is finding a beneficial mutation. (See: Those Elusive Beneficial Mutations.) Geneticists claim 0.1 per cent of them are beneficial. Okay, lets go with it.
Cranking out the numbers shows that on the average one out of every 500,000,000 (500,000 X 1,000) single-celled organisms may have a beneficial mutation. Which brings to question: How long did it take these life forms to build up to a population of 500,000,000?
Evolution by mutation is full of hazards and complications. Here is one: Most animals don't live long enough to reproduce. Something, usually another animal, comes along and kills them before they reach maturity.
Infant mortality varies greatly from species to species. We know that as far as sea creatures go, only a few, just a small percentage, survive to mate. In general, the smaller the creature, the less chance it has to make it to adulthood. How does that affect evolution? It simply adds another hurdle to the list.
All mutations are rare; much rarer are the positive mutations. Now we see that the majority, probably the vast majority of those already extremely rare mutations are dead on arrival. Predators, disease, fire, drought, famine, floods, and other natural disasters destroy them before they have an opportunity to pass on their innovative trait.
Let's think positively. Say we have a one in five hundred million positive mutant who avoids predators, disease, etc. Is he able to pass on his positive mutation? Not necessarily.
Many mature males are barred from finding a mate due to a local dominate male who keeps all available females for himself. That is true for seals, antelopes, baboons, and many other mammals. Obviously, if the positive mutation winds up in a male who can't mate, the beneficial trait will go no further.
Any other roadblocks? Yes, most animal populations are genetically stable. Why? Mates with medium characteristics or traits are favored, while those with unusual traits are shunned. So the majority of individuals in practically all species show intermediate height, weight, and appearance. The range and distribution of traits remain approximately the same from generation to generation. This stabilizing influence is very common.
Some insects, birds, mammals, and other organisms practice "reverse discrimination" and prefer mates who are rare. The beautiful bird plumage in the Paradise Islands is a striking example. But that is the exception.
There is another very strong force for countering chance. Any large population of animals has a natural tendency towards stabilization. A solitary genetic contribution, even a beneficial one, is likely to be swallowed up in a massive gene pool. In the long run, all mutations - good or bad - have no affect on a large population. That is why herd animals remain so constant.
Scientists call it genetic homeostasis. The only place where any mutation stands a chance of surviving is in a small, isolated, peripheral population.
All of this throws a wrench into evolution's gears. Mutations of any sort are rare; mutations which might help evolution are much rarer still; and the bearer of those good-for-evolution mutations are likely to be destroyed by "mother nature" before the innovation can be passed on.
Even if the animal survives to mate, the odds are against his offspring living long enough to permanently establish the new trait in the gene pool. If the bearer is a male, chances are the positive mutation will go no further unless he happens to be the dominate male in the area.
If one of those ever so rare positive mistakes hit a large population, it sinks without a trace. Even if the beneficial mutation winds up in a not-so-large gene pool, the animals will more than likely consider it extreme and discriminate against it.
We will conclude our study with an analogy of evolution by mutation called "The Language of Life": see Evolution:The Devil Is in the Details (Part Four of Four.)
About the Author
Jerry Boone, Gatlinburg, Tennessee, United States webmaster@merechristianity.us Mr. Boone is a sailor, author, and webmaster of http://merechristianity.us His works include: Mere Christianity.us and SAFETY LINE - EVIDENCE OF THINGS NOT SEEN, an apologetic study published 1998.
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