In this post, I consider both mutation and natural selection- two primary evolutionary mechanisms- in the context of driving microevolution and ultimately, macroevolution. By microevolution I mean minute evolutionary change, involving a small proportion of DNA. For example, the peppered moth (biston betularia) in comparison to its non-peppered cousin, would demonstrate microevolution. The former arose in coal-producing regions as an adaptation which made it much more difficult for predators to identify. Because of this it was able to acquire a higher relative fitness, and hence greater survival rate, than its non-peppered cousin.
Of course, microevolution can also appear at the microscopic level, for example in changes in hemoglobins, and histo-compatability antigens. However, it is important not to confuse microevolution with molecular evolution.
The latter includes the following different forms:
-
Base
substitution, whereby one amino acid (nitrogenous base) is replaced by another.
This is called point mutation.
-
Deletion
of a group of bases.
-
Addition
of a group of bases, e.g. if there are multiples of three, one or more amino
acids may be deleted from the protein.
- Inversion, or removal of a segment of DNA accompanied by reinsertion elsewhere but in inverted order. Related to inversion in a way is translocation, wherein a portion of DNA is attached to a homologous chromosome.
In each of the molecular cases above the alteration results in subtle changes in the coding of information or the transfer of information. The molecular changes then act as sources of genetic variation and ultimately evolution i.e. if the change is reinforced by natural selection. Yunis and Prakash, in their groundbreaking
work for example, have shown a remarkable homology between chimp and human
chromosomes, when heterochromatin is excluded. This includes no less than
thirteen ‘presumably identical chromosome pairs’.[1] They
also show that for the common ape-human ancestor, from which both chimps and
modern humans arose, eighteen chromosome pairs were similar to Homo sapiens,
and fifteen to the chimpanzee. They also found that chromosome 17 in the chimp
differs by a ‘pericentric inversion’ from that of man.[2]
Macroevolution, by contrast, entails a large proportional change in the DNA underlying it that probably reflects ongoing natural selection, over significant time. For example, the change from a cold-blooded dinosaur to a warm-blooded dinosaur (that’s a precursor of modern birds) would be a case of macroevolution. Similarly, the change from an ape-human ancestor to Homo sapiens would be a case of macroevolution, despite the fact the evidence is available at the chromosomal level.
Prior to proceeding, let's be clear about
mutation and natural selection in an evolutionary context. A mutation, to be sure, is primarily a random
change induced either spontaneously in the organism's DNA, or from an external
agency (e.g. cosmic rays, x-radiation).
In either case, an accidentally-triggered change at the molecular level
precedes it. This has the effect of altering the DNA information coding process
and the protein synthesis that ensues.
Specific manifestations of mutation can assume the form of one or more of the following:
-
chromosome multiplication: the organism acquires
more than the diploid number of chromosomes
-
chromosome fragmentation: the diploid number of
chromosomes remains constant, but morphological changes take place in one or
more
-
Repetition: portions of chromatin
associated with particular traits occur in different parts of the same
chromosome
-
gene mutation: spontaneous changes at a
gene’s location with no associated alteration of chromosome structure or
number.
Let's examine now how natural selection is able to produce a new bedbug species via microevolution.
In terms of the concept of fitness let B refer to a favored allele for a bedbug
with total resistance (i.e. such that it produces abundant amounts of the
pesticide-resistant enzyme that converts toxins to water-soluble, harmless
excretions), let b refer to a deleterious allele, i.e. one with zero capacity for
such enzyme production.
Recall the measures for success of natural
selection are the fitness (w) and the selective value (s). These can be
measured on either absolute or relative scales, but are related algebraically
on the latter by:
w = 1 – s, or s = 1 – w
Let’s say at a particular time a gene frequency
‘snapshot’ of the bedbug population under study yields: p(B) = 0.60, q(b) =
0.40, i.e. the favored allele B is reproducing bugs at the ratio 3:2 relative
to the disadvantaged one, b. As before, the selective value s = 0.50. (A simple
table showing the declining gene frequency of b relative to B is shown appended
to this blog.)
On average over time let each bb and Bb individual
produce one offspring, and each BB produce two. These average numbers can be
used to indicate the genotype’s absolute fitness and to project the changes in
gene frequency over succeeding generations. The relative fitness (w) is
meanwhile given by:
w = 1 for BB
w = 0.5 for Bb
w = 0.5 for bb
The selection values, relative measures of the
reduction of fitness for each genotype, are given respectively by:
s = 1 – 1 = 0 for BB
s = 1 – 0.5 = 0.5 for Bb
s = 1 – 0.5 = 0.5 for bb
As we expect, the pesticide-resistant bedbug
genotype displays zero reduction in
fitness, and hence maximum survival rate. Thus, the table provides a brief “snapshot” of how
micro-evolution has been working in the bedbug population to generate billions
of these pests that can’t be exterminated by ordinary pesticides –
necessitating the use of varieties currently prohibited for safety and health
reasons.
Let's now use the preceding template and get more
specific (via defined relative populations) as to how the natural selection
mechanism works in enhancing gene frequencies for survival.
We consider a diploid population of 200 individuals, and 400 genes distributed amongst
them. As we see from the table given the ratio of gene frequencies between the
homozygous dominant allele (B or enzyme-resistant to most pesticides) and the
homozygous recessive allele b is 3:2 or 0.60: 0.40 which could manifest for the
case shown via:
B = 180 (in BB) + 60 (in Bb) = 240/400 = 0.60
B = 100 (in bb) + 60 (in Bb) = 160/400 = 0.40
For the 200 individual bedbugs we may also find
the genotype frequencies such that 90 are dominant (resistant to all known
approved pesticides) = 90, and the heterozygous Bb = 60 and the recessive (not
resistant) = bb = 50, therefore for the dominant and recessive allele
distributions using genotype frequencies:
B = 0.45 BB + ½(.30Bb) = 0.45 + 0.15 = 0.60
b = 0.25 BB + ½(.30Bb) = 0.25 + 0.15 = 0.40
Now, for a STABLE population, IF the gene pool (of
a selected population, whether bedbugs, roaches or fruit flies) remains
constant from one generation to the next then the Hardy Weinberg theorem
applies and genetic variation is retained from one generation to the next. We
say the population is in “stasis” and there is NO micro-evolution occurring.
(Note again, the letters p and q in the table denote the two alleles in the
population, i.e. p = B, q = b, thus if B is found to enhance or increase over b
then p will increase over q and we will have micro-evolution, which is exactly
what we see as we go from the top down in the table).
What natural selection does then is to consolidate particular random mutations into a more stable, adaptive
adjustment – governed by deterministic factors and inputs. Thus, while the
selected trait often appears at random, its preservation in the gene structure
cannot be relegated to randomness.
In other words, once the trait – say ligand
recognition by a protein- is incorporated, and gene frequencies increase, the
process ceases to be random. The failure here is being unable to recognize the
distinctions between the condition leading to the initial mutation and the subsequent natural selection
consolidating it into higher gene frequencies!
For a successful mutation deemed to have taken hold and become consolidated in an organism via natural selection, we expect that the fitness w = 1, while there is little or no reduction in selection value, so that s remains near 0 for the most favorable alleles. (For example, resistance to antibiotics.) This is the basis for ongoing evolution. Finally, we can do not better than to present Richard Dawkins' words from The Blind Watchmaker, p. 317:
"The theory of evolution by CUMULATIVE NATURAL SELECTION (emphasis mine) is the ONLY THEORY we KNOW OF that is capable of explaining the existence of organized complexity. Even if the evidence did NOT favor it, it would still be the BEST THEORY available. In fact the evidence DOES favor it, but that is another story.
Let us hear the conclusion of the whole matter. The essence of life is statistical improbability on a colossal scale. Whatever is the explanation for life , therefore , it cannot be by chance . The true explanation for the existence of life must embody the very antithesis of chance. The antithesis of chance is NONRANDOM SURVIVAL, properly understood.
Nonrandom survival, improperly understood, is not the antithesis of chance, but chance itself. There is a CONTINUUM CONNECTING THESE TWO EXTREMES, and it is the continuum from single step selection to cumulative selection. Single step selection is just another way of saying pure chance. This is what I mean by nonrandom survival improperly understood.
CUMULATIVE SELECTION, by slow and gradual degrees, is the explanation, the ONLY WORKABLE explanation for the existence of life's complex design"
See Also:
[1]
Yunis, J. and Prakash, O: 1982, The Origin Of Man- A Chromosomal Pictorial Legacy, Science, Vol. 215, p. 1525. The chromosomes are: 3, 6 to 8, 10, 11, 13, 14, 19 to 22 and XY.
[2]
Ibid.
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