Contents Updated: Monday, September 13, 1999
Professor John Fincham of Edinburgh University, Scotland writes, the spontaneous mutation frequency of an organism is to a large extent controlled by its own genotype.
In other words organisms mutate at rates controlled by their own genes. Precisely. The saltagen controls the mutational rate.
We know organisms have genes called antimutator genes which provide mechanisms to repair DNA chains that have replicated wrongly. These DNA repair and mutation avoidance mechanisms work thus: the faulty bit of DNA is tagged by some suitable chemical sidechain, specific chemicals called enzymes seek out the tag, cut out the faulty part and replace it with the correct piece.
A gene observed in the gut bacterium, E. coli, is called Treffers Gene. Normally it acts as an antimutator gene, but it too is subject to mutation. When it mutates its effectiveness in suppressing mutations in other genes decreases, making the rate of mutation of these genes rise a hundred times.
Here we have a gene which, when mutated causes other genes to mutate more. A saltagen?
Another mechanism operates while the DNA chain is replicating. DNA polymerase, an enzyme that has the function of building the DNA polymer, checks the chain as it is being built. It proof reads each copy of the genetic code. If the last monomer it added matches the DNA template, the unraveled DNA strand from the previous generation, then a new monomer is added. If it does not match, the DNA polymerase cuts the previous monomer away and replaces it with a correct one.
But certain mutations affect the DNA polymerase itself, rendering it not such a good proof reader. The result? More mutations of the genes during their construction!
Many DNA sequences have more than one function. They can be read more than once with different results. My milkman sees a message by my doorstep saying, No milk today with a pointer that can be directed at the word No or the word milk. If it points to the No" I get no milk but if it points to the milk, I get milk. The code No milk today does not alter but the outcome depends on where the message starts.
That illustrates one way that one stretch of DNA can be read differently. Another way would be to read it in a different order, akin to reading the word STAR (forwards) or RATS (backwards).
The way in which the bit of code is read is determined by a previous bit of code. Errors in these instructions can have profound effects on the meaning of a genetic sequence and thence on the macro features of an organism.
An example is the pseudogene for production of globin, a protein, in humans. Pseudogenes are decayed genes. The pseudogene for globin is all but identical to active genes for globin production but have mutated in their initiation codon, the piece of DNA coding sequence saying where the message starts, and also in other parts of the code. In short, the mechanism for reading the gene no longer operates.
It seems a piece of DNA containing the active globin gene mutated by doubling then one of the bits fell out of use, remaining only as redundant code.
What causes plagues? I am not digressing. The answer provides an interesting example of the effect of a copying error and switching off a gene.
Hans Wolf-Watz of the University of Umea in Sweden and his team have looked at the DNA sequences of the plague bacterium, Yersinia. Normally this bacterium is not very virulent, but occasionally a copying error occurs in which one letter of the code is lost thus scrambling a whole coding sequence. The function of that part of the code is not known but the effect of the error gives a clue—the mutant bacterium is deadly. The piece of code helps the host to defend itself against the bacterium.
Why should it do that? Simply because by not doing, it kills off its hosts rapidly leaving it with nowhere to live—it too dies. With the bit of protective code active the host is likely to survive and the bacterium with it. The protective sequence is in a part of the code that has a high mutation rate so deadly mutants are thrown up quite often, but plague epidemics are not very frequent. The reason is that the virulent form of Yersinia normally kills its host before it has had time to be transmitted to another. Only in overcrowded and unsanitary conditions is it able to spread from one host to another before the hapless host is done in.
The rapidly mutating piece of code looks as though it switches on occasionally to test the environment. If it is suitable—conditions are overcrowded and unsanitary—the virulent bacterium spreads rapidly but otherwise it dies out for awhile until reborn by a replicating error. A gene which switches on to test the environment—just like a saltagen!
Even more relevant may be a phenomenon called replicating instability which, unlike the examples just mentioned, seems to be a positive effect rather than a negative one, although it is not yet understood. It seems to allow a propensity to mutate to transmit through an indefinite number of replications before, for some reason, it manifests itself. Isn't that another gene that is switched off until the conditions are right?
Earlier we speculated about an incest gene. If there were such a thing it could, once it had turned on, remain switched on so that it actually provided the distinguishing feature of the new species. Linked to some physical characteristic it would be recognizable by all others possessing the gene, drawing them inexorably into mutual reproduction.
As more creatures were born with the gene, it would cease to cause incest because others not in the immediate family would also carry the gene. It will have become a breeding preference distinguishing two populations and eventually leading to speciation.
Alternatively, perhaps like the saltagen, it turns on under environmental pressure for change—in other words when there is a need for rapid evolution. This could have been true of certain apes in the last ten million years or so, judging by the successive waves of hominids appearing until the Cro-Magnon variety, only a few tens of thousands of years ago. Either way it can permit speciation when it might not be expected and therefore speed up evolution.
Jane van Lawick Goodall has noted that chimpanzees and other primates show no sexual interest in their mothers. Yet men seem obsessed by the Oedipal complex. That man carries the incest gene unlike his primate cousins might be the key distinction between them. Have we evolved rapidly because we are the Oedipal ape?
Impressive testimony to the existence of a fast-acting mechanism for creating extra bits of DNA sequence, according to Fincham, is the behavior of cells cultivated in the drug methotrexate. An excess of this drug, which inhibits one of the cell's enzymes, in the environment causes the cells to develop enormously lengthened chromosomes carrying multiple repeats of the DNA segment for production of the enzyme. In response to the intense selection pressure of the harmful drug, the cell repeatedly mutated by doubling the satellite sequence containing the code it needed to manufacture the enzyme under attack.
This is hardly random mutation. Impressive testimony indeed.
Fincham sums up thus: These mechanisms are themselves subject to mutation and natural selection and the spontaneous mutation frequencies which we find in natural populations of organisms of all kinds are adaptive. They presumably represent a compromise between short-term need to replicate already well adapted DNA sequences with sufficient precision and the longer term advantage of variability.
The mutation rate per gene is only one per million replications but, because a lot of genes are needed to define an organism, that makes mutation quite likely in the whole DNA sequence. Large organisms average about one mutation in ten replications many of which, we have noted, are harmful and most of those that are not are neutral. This may be near the acceptable limit for human DNA. More complex DNA would mutate too often making reproduction unreliable. Hence beyond this level of complexity, evolution favors the storage of information in the brain rather than in the genes.
By comparing the amount of information estimated to be in the genes of different types of animal with the amount of information estimated to be in their brains, Carl Sagan deduces that somewhere in the steamy jungles of the Carboniferous Period animals emerged with more information in their brains than in their genes. This estimate is quite imperfect because the information is imprecise and the figures cover a large range requiring logarithmic relationships which exaggerate errors. But, though the date of the crossover is inexact, the notion seems valid.
Since the crossover point, whenever it was, brains have increasingly dominated genes. This suggests there might be a threshold beyond which evolutionary pressure builds up to develop brain rather than extend the complexity of the DNA. Some dinosaurs, having passed the threshold, might have built up an evolutionary head of steam for intelligence.
Evolution is faster for birds and mammals than for the cold blooded amphibians, fish and reptiles. At the annual meeting of the British Association for the Advancement of Science in 1988 Allan Wilson, of the University of California at Berkeley, proposed that animals with larger EQs evolve faster than less brainy relatives. Wilson believes the increase in brain size accounts for their difference in evolutionary speeds. If true then one can expect an explosive evolution of the brain by positive feedback.
To measure evolutionary differences, Wilson took 20,000 bone measurements from 400 species of vertebrates. From these results he created an index of how different the shape of the body was for any two vertebrate species. Closely related species like the coal tit and the blue tit had an index of 3 whereas the differences between an eagle and a sparrow were reflected in their index of 25. Combining this index with the date of separation of species using the molecular clock allowed Wilson to plot evolutionary change against time.
He found that evolution is speeding up. His explanation is that brains drive evolution:
As brains became bigger and bigger they became the predominant cause of the pressure to evolve.
More intelligent species are more willing to try new forms of behavior and that gives more scope for selection to operate. When a group of animals have learnt a new behavior then evolution will change their physical attributes the better to take advantage of the new behavior. Animals evolve more quickly when their brains are advanced enough to allow them to modify their behavior. The creature's body then evolves along the lines best suited to the new behavior pattern.
Because the brain is both one of the physical attributes subject to evolution and a factor controlling the rate of that evolution, a chain reaction occurs by positive feedback. The result is exponential growth—growth which is at an ever increasing rate. Wilson believes that innovation and imitation among our hominid ancestors provided selective pressure for physical changes including greater brain size.
Those lineages with larger brains evolve more and more quickly, and eventually you get a species which is so intelligent that cultural evolution takes over entirely from genetic evolution.
Science writer, Nicholas Schoon, adds that our ape-like ancestors of the past few million years:
have undergone one of the fastest rates of evolution on record. The brain almost trebled in size, the larynx, tongue and lips changed as speech developed, the thumb and fingers altered so that we could manipulate tools with precision, and walking on two legs was perfected.
According to Wilson, it is inevitable that overwhelmingly intelligent species should dominate the planet. If humans were to die out another mammal or a bird, would replace us.
Since exponential growth is steady continuous growth but at an ever increasing rate, for a very long period both size and growth rate are so small that changes can hardly be noticed, but eventually the growth rate seems to take off, as if it had passed a threshold.
This is just what we see in the growth of intelligence. It is as if, in our evolutionary hyperspace, intelligence is a lake at the bottom of a trough with steeper slopes the closer the approach to the surface of the lake. You slip down the slope gathering momentum until you tumble over the edge. Any creature getting to the edge will find itself precipitated into the Sea of Knowledge.
There are conflicting views about how easily intelligence evolves. Some say it is rare yet I argue that species are accelerating towards ever higher intelligence.
The conflict is explained by the hazards of getting to where the slope starts perceptibly to incline towards the sea of knowledge. There are many other comfortable troughs that species can settle in before it gets to the edge, just as a golfer might find it difficult to get on to the green without getting trapped in a bunker—and this is not a par five hole: it has countless dog legs and bunkers on the way.
The many species that have existed on earth without developing intelligence couldn't get out of the bunkers. So far, not many have got to the green, the equivalent in the golfing analogy to the sea of our landscape analogy.
What is clear is that, given certain attributes, intelligence seems bound to evolve—and quickly. Some dinosaurs seem to have had those attributes and could have developed rapidly, just as we have.