What does the future hold for us as a species? Whatever challenges we may face in the future, a remarkable study in Nature shows how prefabricated solutions may already exist in our genes.
In the report, Suzanne L. Rutherford and Susan Lindquist of the Howard Hughes Medical Institute at the University of Chicago show how genes important in regulating growth and development may accumulate mutations silently. But when a species is faced with environmental crisis, these mutations may be suddenly unleashed. This burst of mutation will produce a wider range of forms than usual on which natural selection can act, increasing the chance that a species can get through hard times and adapt to changed circumstances even if altered in new and interesting ways.
This research could provide answers to pressing problems in evolutionary studies, such as how the normal, slow process of gradual evolutionary change the kind of change that Darwin envisaged in his 1859 book On The Origin Of Species can account for the origin of dramatically new kinds of 'body plan'. For example, the fossil record suggests that most major kinds of animal, ranging from molluscs to vertebrates (backboned animals) to arthropods (jointed legged animals) originated between 600 and 500 million years ago, in a burst of evolutionary activity unmatched by subsequent events.
There is currently debate about the timing, nature and where to get pandora bracelet even the existence of this pulse of evolution, called the 'Cambrian Explosion'. But the fact remains that the mechanism of natural selection has a hard time explaining how radical alterations in animal shape and form can take place within a relatively short period of time. A hundred million years may seem like an eternity but no major animal body forms have appeared since the Cambrian jewelry pandora bracelet Explosion.
What was different about evolution in the Cambrian compared with evolution since? Some researchers have sought answers in embryology, the biology of growth and development.
It is one of life's wonders that the fertilized yet formless egg of an animal of a given species always grows up into another individual of that species, and not into something else. Jeff Goldblum in The Fly aside, why can human mothers be relied upon to produce human babies, and not cats, dogs or giraffes? We take this continuity so much for granted that even asking such a question seems strange. There is an increasing awareness that this reliability is enforced by networks and cascades of regulatory genes, and that the large scale pattern of evolution might be sought in comparisons between these networks in species of different body plans worms or fruit flies compared with humans or mice, for example.
Although the past ten or fifteen years have seen dramatic advances in our understanding of developmental pathways, we still know too little to give any more than the sketchiest explanations of the pattern of evolution in terms of development. But some researchers have speculated that animal life in the Cambrian was still newly evolved enough that the developmental control pathways we now take for granted may have been somewhat looser than they are now. Lax control might have produced, routinely, a greater range of variation in form than we would expect nowadays. A larger range of variation offers more scope for natural selection to sculpt animal forms to suit their environment especially if the environment changes rapidly and in unexpected ways.
The problem has always been that no really plausible mechanism has been put forward in which looseness of developmental control could be translated into a dramatic and possibly sudden burst of evolution. Rutherford and Lindquist may now have taken an important step towards creating a model for that mechanistic connection.
They have been looking at a protein called Hsp90. This is a member of a ubiquitous family called the 'heat shock proteins' (hence 'Hsp'). These proteins are molecular minders: they assist newly formed proteins in assuming their mature shapes, as having the correct shape is vital for the function of all proteins. But they also brace proteins against the effects of unusual hazards, such as high temperature. Work on organisms from flies to yeast shows that when the heat is on, heat shock proteins bind to other proteins, helping them keep in shape. But heat shock proteins are known that protect against a range of other hazards, such as oxygen starvation, damage caused by highly reactive 'free radicals' and even some chronic degenerative diseases. In other words, heat shock proteins protect an organism against a variety of stresses, so they could really be called 'stress proteins'.
Hsp90, though, has another function. That is, it binds to a range of proteins that happen to be important in a variety of biochemical pathways concerned with cell division, growth and development. Many of these proteins are inherently unstable. By repeatedly binding to and detaching from these proteins, Hsp90 keeps them in an unstable state on the boil ready to discharge their function without going off prematurely.
Crucially, Hsp90 is not sensitive to the precise form of these proteins, but responds in a more general way to overall features that suggest their instability. In the same way that an efficient Best Man will get the Bridegroom to the wedding on time, irrespective of the nature or severity of the effects of the bachelor party, Hsp90 is 'concerned' if one might be teleological, for the sake of elision with keeping an unstable developmental control protein in readiness, irrespective of the precise nature or function of that protein.
This means that developmental control proteins can accumulate mutations slight changes in sequence and form but that these mutations are masked by the efficacy of Hsp90 in ensuring that the control proteins get to do what they are supposed to.
Rutherford and Lindquist have been looking at strains of fruit flies (Drosophila), in which Hsp90 is disabled either by mutation of by the effects of a drug. In the absence of functional Hsp90, flies threw up a greater than normal proportion of unusual mutants flies with eyes of different colours and shapes from normal, or with no eyes at all; flies with abnormally shaped wings and legs; flies with body parts transposed to places they weren't supposed to be, and so on.
Mutant flies are nothing new in biology, but two things make this work stand out. First, the kinds of mutations weren't related to the loss of Hsp90, and they weren't totally random instead, they were related to the 'genetic background' of the stock from which the parents of the mutant flies came. This suggests that nile jewelry the lack of Hsp90 was releasing a Pandora's Box of mutations acquired by particular fly lineages, but which remained hidden until such time as the control exercised by Hsp90 was relaxed.
Second, mutant flies could be bred to maintain the mutations in the population, and the mutations would persist even in progeny in which Hsp90 was, once again, functional. In other words, once the mutations were out of Pandora's Box, they could not always be coaxed back in again. An episode in which Hsp90 was removed from the picture resulted in the irrevocable change of the body form of the fly.
How could this happen in real life? A clue came from experiments showing how mutations were more common when flies were reared at higher temperatures. In times of stress, Hsp90 has to work double time as a 'chaperone' of unstable developmental control proteins, and as a general purpose stress protein. At times of crisis, Hsp90 is diverted from the first task to the second, allowing the hidden mutations in developmental control proteins to be expressed.
In evolutionary terms, it is precisely at such times that a population needs to display as much overt variation as it can, to give plenty of fuel for natural selection to hone it to fit changing circumstances. "Uniquely, Hsp90 links the response to environmental stress with control of development," writes Andrew Cossins of the University of Liverpool, UK, in a commentary on the Rutherford and Lindquist report, "providing a means by which increased environmental variability might be countered by more variety in the form and function of an organism."
The work by Rutherford and Lindquist is, at the moment, a laboratory model for how the environment and development could be connected in a way that could influence evolutionary change. Nobody is suggesting that Hsp90, in particular, is the key to evolution. But as a result of work like this, researchers will now be looking more intently at stress proteins, and how proteins in general interact to regulate development.
A mechanism like this, in which mutations in developmental control rgimes are stored silently away until brought out by episodes of environmental crisis, provides for the first time a general model for the kind of rapid, large scale evolutionary change that palaeontologists see in the fossil record in, for example, the Cambrian Explosion. At the start of the Cambrian period, 543 million years ago, the world had just endured the greatest, most extensive Ice Ages of its entire history. Profound changes were occurring in the biosphere. In particular, the concentration of molecular oxygen in the atmosphere was rising.
This has been suggested as a spur for the evolution of large animals large enough to be seen, at least, with the naked eye but the mechanism has been elusive. Could the stress of rising price of a pandora charm oxygen have released the mutations necessarily to drive the origin of body plans?
Such questions are, for the moment, speculative in the extreme. And yet, for the first time, we are now in a position to start framing answers in terms of actual molecular mechanisms.
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