Manual A Silent Gene Theory of Evolution

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Add to cart. Be the first to write a review About this product. About this product Product Information Two distinguished scientists encouraged Warwick Collins in writing his revolutionary theory of evolution. Professor Freeman Dyson, one of the world's leading theoretical physicists, wrote, "I like your theory, and think it has a good chance of being right. I agree, therefore, that if silent gene theory were proved correct, it would be the more complete theory, as Einstein's is compared with Newton's.

What then is the true source of variation in evolutionary systems? It is a question which has obsessed Warwick Collins, a novelist who had studied biology at university, for much of his adult life.

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He proposed in March that the required degree of variation could be achieved if large numbers of inert or silent genes existed within the genome. Such genes, because they do not code for physical characteristics, could freely mutate over time without deleteriously affecting the host organism.


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At a later stage they could be switched on, by largely random processes, and generate exotic new variants. Remarkably, his description of silent genes was found to correspond precisely with the so-called junk genes.

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These are found in all species, forming the great majority of genes in multicellular species and rising to Until then their function had proved mysterious. In addition, Collins's theory predicted a number of features of the silent or junk genes which have since been increasingly verified by recent research: for example, that they could become active and begin to code, and that they influenced other genes.

It is now widely accepted that, just as Collins predicted, the vast majority of significant mutation in the genomes of complex species arises from the silent genes. But Collins's powerful and ambitious theory moves well beyond the molecular realm.

The Silent Gene: A New Theory of Evolution

He argues that while natural selection is a major force in evolution, it is primarily negative and entropic. Instead, the great driver of complex evolution is the range of variation created by the silent genes. As Professor Donald Braben writes in his illuminating foreword, "Collins is proposing a general evolutionary theory which, if it continues to be supported by the data, may in due course come to rival Darwin's theory that evolution is driven by natural selection.

Additional Product Features Dewey Edition. He argues that the so-called "junk DNA" consists of silent genes that are not subject to the normal processes of natural selection and thus can evolve freely over long periods of time without adversely affecting the host organisms. He further argues that a strong theory of variation as the driver of evolution provides a better general theory of evolution than Darwin's theory that evolution is driven by natural selection.

Previously unavailable in the US. Show More Show Less. No ratings or reviews yet. Be the first to write a review. Best Selling in Nonfiction See all. Unfreedom of The Press by Mark R. Trivers argued that families create an evolutionary conflict. Natural selection should favor parents who can successfully raise the most offspring. For that strategy to work, they can't put too many resources into any one child. But the child's chances for reproductive success will increase as its care and feeding increase. Theoretically, Dr. Trivers argued, natural selection could favor genes that help children get more resources from their parents than the parents want to give.

As Dr. Haig considered the case of pregnancy, it seemed like the perfect arena for this sort of conflict. A child develops in intimate contact with its mother. Its development in the womb is crucial to its long-term health. So it was plausible that nature would favor genes that allowed fetuses to draw more resources from their mothers. A fetus does not sit passively in its mother's womb and wait to be fed.

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Its placenta aggressively sprouts blood vessels that invade its mother's tissues to extract nutrients. Meanwhile, Dr. Haig argued, natural selection should favor mothers who could restrain these incursions, and manage to have several surviving offspring carrying on their genes.

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He envisioned pregnancy as a tug of war. Each side pulls hard, and yet a flag tied to the middle of the rope barely moves. Haig said. In a paper, Dr. Haig first predicted that many complications of pregnancy would turn out to be produced by this conflict. One of the most common complications is pre-eclampsia, in which women experience dangerously high blood pressure late in pregnancy.

For decades scientists have puzzled over pre-eclampsia, which occurs in about 6 percent of pregnancies. Haig proposed that pre-eclampsia was just an extreme form of a strategy used by all fetuses. The fetuses somehow raised the blood pressure of their mothers so as to drive more blood into the relatively low-pressure placenta. Haig suggested that pre-eclampsia would be associated with some substance that fetuses injected into their mothers' bloodstreams. Pre-eclampsia happened when fetuses injected too much of the stuff, perhaps if they were having trouble getting enough nourishment.

In the past few years, Ananth Karumanchi of Harvard Medical School and his colleagues have gathered evidence that suggests Dr. Haig was right. They have found that women with pre-eclampsia had unusually high levels of a protein called soluble fms-like tyrosine kinase 1, or sFlt1 for short. Other labs have replicated their results. Karumanchi's group has done additional work that indicates that this protein interferes with the mother's ability to repair minor damage to her blood vessels.

As that damage builds up, so does her blood pressure. And as Dr. Haig predicted, the protein is produced by the fetus, not the mother. Haig is now collaborating with Dr. Karumanchi and his Harvard Medical School colleagues to understand more about how exactly sFlt1 may cause pre-eclampsia.

They describe their research in the latest issue of Current Topics in Developmental Biology. Haig also made some predictions about the sorts of maternal defenses that have evolved.

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One of the most intriguing strategies he proposed was for mothers to shut down some of the genes in their own children. This strategy takes advantage of the fact that most of the genes we carry come in pairs. We inherit one copy from our mother and one from our father. In most cases, these pairs of genes behave identically. But in the past 15 years, scientists have identified more than 70 pairs of genes in which the copy from one parent never makes a protein.

In some cases, a parent's gene is silenced only in one organ. View all New York Times newsletters. Scientists do not fully understand this process, known as genomic imprinting. They suspect that it is made possible by chemical handles called methyl groups that are attached to units of DNA. Some handles may turn off genes in sperm and egg cells. The genes then remain shut off after a sperm fertilizes an egg. Only a few of these genes have been carefully studied to understand how they work. But the evidence so far is consistent with Dr. Haig's theory. One of the most striking examples is a gene called insulin growth factor 2 Igf2.

Produced only in fetal cells, it stimulates rapid growth. Normally, only the father's copy is active. To understand the gene's function, scientists disabled the father's copy in the placenta of fetal mice. The mice were born weighing 40 percent below average. Perhaps the mother's copy of Igf2 is silent because turning it off helps slow the growth of a fetus.

On the other hand, mice carry another gene called Igf2r that interferes with the growth-spurring activity of Igf2. This may be another maternal defense gene. In the case of Igf2r, it is the father's gene that is silent, perhaps as a way for fathers to speed up the growth of their offspring. If the mother's copy of this second gene is disabled, mouse pups are born percent heavier than average. A number of other imprinted genes speed and slow the growth of fetuses in a similar fashion, providing more support for Dr. And in recent years, some medical disorders in humans have been tied to these imprinted genes.

Beckwith-Wiedemann syndrome, for example, causes children to grow oversize organs that are prone to developing tumors. Some cases of the disorder have been tied to a mutation that replaces a mother's silent copy of Igf2 with an extra copy of the father's. The extra Igf2 appeared to cause a fetus to grow too quickly, leading to the syndrome. Haig's work is now widely hailed for making sense of imprinted genes. Haig has recently been exploring his theory's implications for life after birth.

Scientists have found that some genes are imprinted in the brain after birth, and in some cases even in adulthood. Lawrence Wilkinson of the University of Cambridge.