Most books that describe evolution seem to assume that every time there's a mutation, the environment promptly gets to judge it good or bad ... but one little trick, HSP90, which is present in most animals and many bacteria, makes nonsense of that assertion. And from Lewontin's discovery that a third of genes have common variants in wild populations, and that all organisms carry lots of them, it is clear that ancient mutations are continually being tested in different modern combinations, while the potential effects of more recent mutations are being cloaked by HSP90 and its ilk.
The trick employed by mammals is much more complex and farreaching. They reorganised their genes, and got rid of a lot of genetic complication that their amphibian ancestors relied on, by adopting a new and more controlled developmental strategy. Most frogs and fishes, whose eggs usually encounter great differences and changes of temperature during each embryology, ensure that the `same' larva, and then adult, results. Think of frog spawn in a frozen English pond, warming up to 35°C during the day while the delicate early development proceeds; then the little hatchling tadpoles have to endure these temperature changes. Now think of the frogs that so few of the tadpoles become.
Most chemical reactions, including many biochemical ones, happen at different rates if the temperature is different. You only get a frog if all the different developmental processes fit together effectively, and timing is crucial. So how does frog development work at all, given that the environment is changing so quickly and repeatedly?
The answer is that the frog genome `contains' many different contingency plans, for many different environmental scenarios. There are many different versions of each of the enzymes and other proteins that frog development requires. All of them are put into the egg while it is in mother frog's ovary. There are perhaps as many as ten versions of each, appropriate to different temperatures (fast enzymes for low temperatures, sluggish ones for higher temperatures, to keep the duration of development much the same) [1], and they have `labels' on the packages that make them, so the embryo can choose which one to use according to its temperature. Animals whose development must be buffered in this way use a lot of their genetic programme to set up contingency plans for many other variables, in addition to temperature.
The mammals cleverly avoided all of this faffing around, by making their females thermostatically controlled -'warm-blooded'. What
[1] That's very important for a few species. Zebra-fish eggs in the wild must hatch in just under 72 hours, because they're laid just before dawn and must hide before the third dawn when predators could see them.
counts is not the warmth of the blood, but the system that maintains it at a constant temperature. The beautifully controlled uterus keeps all kinds of other variables away from the embryos, too, from poisons to predators. It probably `costs' much less in DNA programming to adopt this strategy, too.
This trick, evolved by the mammals, carries an important message. To ask how much information passes across the generations in the DNA blueprint, as textbooks and sophisticated research manuals often do, is to miss the point. How the genes and proteins are used is far more important, and far more interesting, than how many genes or proteins there are in a given creature. Lungfishes and some salamanders, even some amoebas, have more than fifty times as much DNA as we mammals do. What does this say about how complex these creatures are, compared to us?
Absolutely nothing.
Tricks like HSP90, and strategies like warm-bloodedness and keeping development inside the mother, mean that bean-counting of DNA `information' is beside the point. What counts is what the DNA means, not how big it is. And meaning depends on context, as well as content: you can't regulate the temperature of a uterus unless your context (that is, mother) provides one.
The simple-minded `mutation' viewpoint, allied to trendy interpretations of DNA function in terms of `information theory', is often allied with ignorance of biology in other areas. One example is radiation biology and simple ecology as seen by `conservation activists'. Some of these volunteers found five-legged frogs and other 'monsters' downwind of the Chernobyl site, years after the nuclear accident but while radiation levels were still noticeably high. They claimed that the monsters were mutants, caused by the radiation. Other workers, however, then found just as many supposed mutants upwind of the reactor site.
It turned out that the best explanation had nothing to do with mutant frogs. It was the absence of their usual predators, owls and hawks and snakes, because there were so many humans trudging about. Rana palustris tadpoles from Chernobyl produced no more of these pathologies than did other frogspawn samples from ponds some tens of kilometres away that had not been subjected to radiation, when a high percentage of both was allowed to survive. Usually, in British Rana temporaria frogs, it is very difficult to achieve ten per cent normal adults, or even ones that are viable in the laboratory, but they don't produce extra limbs as palustris does. It is normally the case, of course, that a female frog's lifetime production of some 10,000 eggs results in a few highly selected, and therefore `normal', survivors, and on average just two breeders. But conservationists don't like thinking about this reproductive arithmetic, with all those deaths.
Here is another issue, again chosen from the thalidomide literature, that demonstrates how talk of Lamarckism, or of `mutations', misses the point.
Some of the children affected by thalidomide have married each other, and several of these pairings have produced phocomelic children. The obvious deduction, from the folk-DNA point of view, is that the DNA of the first generation must have been altered, so that it produced the same effect in the next generation. In fact, this effect looks, at first glance, like Lamarckism: the inheritance of acquired characters. Indeed, it seems a classic demonstration of such inheritance, as convincing as if cutting off terriers' tails resulted in puppies being born with short tails. However, it is actually a lesson in not attempting to explain things `at first glance', like the conservationists did with the abnormal frogs.
It is very tempting to do just that, when the idea of heredity in your mind is that one gene leads to one character, so if you've got the character you've got the gene, and vice versa. Figures from the epidemiological literature suggest that in the space of a few years either side of 1960, about 4 million women took thalidomide at the critical time during gestation. Of those, about 15,000-18,000 foetuses were damaged; 12,000 came to birth with defects, and about 8,000 survived their first year. That is to say, the natural course of development selected just 1 in 500 who showed adverse effects. The proportion of children born with no detectable defect was much, much higher. And that fact changes our view of the likely reason for the children of two thalidomide parents to suffer from phocomelia, for the following reason.
Conrad Waddington demonstrated a phenomenon called `genetic assimilation'. He started with a genetically diverse population of wild fruit flies, and found that about one in 15,000 of their pupae, when warmed, produced a fly with no cross-vein in its wing. These 'crossveinless' flies looked just like some very rare mutant flies that turned up occasionally in the wild, just as occasional genetically phocomelic children turned up before thalidomide. By breeding from the flies that responded to the treatment, Waddington selected for a lower and lower threshold of response. In a few tens of generations, he had selected flies that bred true for the cross-veinless trait, exhibiting it regularly without anyone warming the pupae. This may look like Lamarckian inheritance, but it's not. It's genetic assimilation. The experiments were selecting flies that had no cross-vein at lower and lower temperature thresholds. Eventually, they selected flies that had no cross-vein at `normal' temperatures.