Evolution – The Devil Is in the Details (Part Three of Six)

Are mutations the driving force in evolution? Is that feasible? Let's do a bit of detective work and see if we can answer these questions.

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 typically 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 sometimes 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 was to mutate into a uriacil (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. Occidentally, 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 trains – color of eyes, skin, hair, or length or shape of the nose, ears, etc.

Often a single human character 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 contributor 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 compared to the 23 pair found in humans.

Changes in the number, size, or organization of chromosomes are called chromosome mutations. Two chromosomes may fuse into one; Or one breaks into two; Egypt 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 became separated and vice versa. Physical hits 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 does not. A mishap at the chromosome level does not crank out new exercises. It sincerely reshuffles old ones. We can not go from bacteria to humans by scrambling chromosomes. It is just another dead end for macroevolution.

Our brief look at mutations really has not 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, however seems promising. Gene mutations produce diseases, monsters, or death, with an incidental neutral result. It is suggested that although on rare rare occasions, something beneficial might occur. That does not seem too encouraging for the bacteria to man scenario.

Even less promising are chromosome mutations which are certainly mix already existing characteristics. So what makes evolution tick?

We will continue our study of mutations with "Mutations: Facts and Figures": see Evolution: The Devil Is in the Details (Part Four of Six.)