Genetic Modification Quotes

Look at them, the bugs. Humans have used everything in their power to extinguish them: every kind of poison, aerial sprays, introducing and cultivating their natural predators, searching for and destroying their eggs, using genetic modification to sterilize them, burning with fire, drowning with water. Every family has bug spray, every desk has a flyswatter under it… this long war has been going on for the entire history of human civilization. But the outcome is still in doubt. The bugs have not been eliminated. They still proudly live between the heavens and the earth, and their numbers have not diminished from the time before the appearance of the humans. The Trisolarans who deemed the humans bugs seemed to have forgotten one fact: The bugs have never been truly defeated. A small black cloud covered the sun and cast a moving shadow against the ground. This was not a common cloud, but a swarm of locusts that had just arrived. As the swarm landed in the fields nearby, the three men stood in the middle of a living shower, feeling the dignity of life on Earth. Ding Yi and Wang Miao poured the two bottles of wine they had with them on the ground beneath their feet, a toast for the bugs.

The possibility of genetic modification reminds me of the need for a scientifically literate electorate. Please stay tuned and vote!

Look at them, the bugs. Humans have used everything in their power to extinguish them: every kind of poison, aerial sprays, introducing and cultivating their natural predators, searching for and destroying their eggs, using genetic modification to sterilize them, burning with fire, drowning with water. Every family has bug spray, every desk has a fly-swatter under it... this long war has been going on for the entire history of human civilization. But the outcome is still in doubt. The bugs have not been eliminated.

Apollo has something to teach us as we enter a new century of genetic modification, artificial intelligence, nanotechnology. It's a cautionary tale about that most fundamentally human of human tragedies .. wanting something so badly that you end up destroying it.

But genetic modification is the same thing humans have been doing for millennia, just with more precision. It actually changes less of a plant’s organic genome than hybridization.

Look at them, the bugs. Humans have used everything in their power to extinguish them: every kind of poison, aerial sprays, introducing and cultivating their natural predators, searching for and destroying their eggs, using genetic modification to sterilize them, burning with fire, drowning with water. Every family has bug spray, every desk has a flyswatter under it… this long war has been going on for the entire history of human civilization. But the outcome is still in doubt. The bugs have not been eliminated. They still proudly live between the heavens and the earth, and their numbers have not diminished from the time before the appearance of the humans. The Trisolarans who deemed the humans bugs seemed to have forgotten one fact: The bugs have never been truly defeated.

The next step in the process of making modern farming more efficient and profitable was genetic modification. In bioengineered plants, lectins are artificially inserted. Scientists selectively add foreign genes into a plant’s basic genome to command the plant to manufacture specific lectins that enhance the plant’s ability to resist insects and other pests. This is one form of genetically modified organisms (GMO).

First Law In every animal which has not passed the limit of its development, a more frequent and continuous use of any organ gradually strengthens, develops and enlarges that organ, and gives it a power proportional to the length of time it has been so used; while the permanent disuse of any organ imperceptibly weakens and deteriorates it, and progressively diminishes its functional capacity, until it finally disappears. Second Law All the acquisitions or losses wrought by nature on individuals, through the influence of the environment in which their race has long been placed, and hence through the influence of the predominant use or permanent disuse of any organ; all these are preserved by reproduction to the new individuals which arise, provided that the acquired modifications are common to both sexes, or at least to the individuals which produce the young.

In a 2008 retrospective paper on the 1975 Asilomar conference that he co-organized—the conference that led to a moratorium on genetic modification of humans—the biologist Paul Berg wrote,16 There is a lesson in Asilomar for all of science: the best way to respond to concerns created by emerging knowledge or early-stage technologies is for scientists from publicly funded institutions to find common cause with the wider public about the best way to regulate—as early as possible. Once scientists from corporations begin to dominate the research enterprise, it will simply be too late.

In the case of food, if the argument is valid that we need some kind of genetic modification to help feed the world’s growing population, then I believe that we cannot simply dismiss this branch of genetic technology. However, if, as suggested by its critics, this argument is merely a front for motives that are primarily commercial—such as producing food that will simply have a longer lasting shelf life, that can be more easily exported from one side of the world to the other, that is more attractive in appearance and more convenient in consumption, or creating grains and cereals engineered not to produce their own seeds so that farmers are forced to depend entirely upon the biotech companies for seeds—then clearly such practices must be seriously questioned. Many

Morgan had discovered an important modification to Mendel's laws. Genes did not travel separately; instead, they moved in packs. Packets of information were themselves packaged-into chromosomes, and ultimately in cells. But the discovery had a more important consequence: conceptually, Morgan had not just linked genes; he had linked two disciplines-cell biology and genetics. The gene was not a "purely theoretical unit." It was a material thing that lived in a particular location, and a particular form, within a cell.

During the war, Monod had joined the Communist Party as a matter of expediency, so that he could join the FTP. But he developed reservations about the Communists’ intolerance of other political views and quietly quit the Party after the war, at a time when many fellow citizens were joining. That might have been the end of Monod’s involvement with Communism, were it not for bizarre developments in the sphere of Soviet science. In the summer of 1948, Trofim Denisovich Lysenko, Joseph Stalin’s anointed czar of Soviet agriculture, launched a broad attack on the science of genetics. Lysenko believed that virtually any modification could be made rapidly and permanently to any plant or animal and passed on to its offspring. His belief, while consistent with Soviet doctrine that nature and man could be shaped in any way and were unconstrained by history or heredity, flew in the face of the principles of genetics that had been established over the previous fifty years. Nevertheless, Lysenko demanded that classical genetics, and its supporters, be purged from Soviet biology. Lysenko’s outrageous statements were heralded in Communist-run newspapers in France. Monod responded with a devastating critique that ran on the front page of Combat. Monod exposed Lysenko’s stance on genetics as antiscientific dogma and decried Lysenko’s power as a demonstration of “ideological terrorism” in the Soviet Union. The public scrutiny damaged the credibility of Soviet socialism in France. The episode thrust Monod into the public eye and made him resolve to “make his life’s goal a crusade against antiscientific, religious metaphysics, whether it be from Church or State.

Government By The Industry, For The Industry Vice President George Bush sat in his chair across from four Monsanto executives. They had come to the White House with an unusual request. They wanted more regulation. They were venturing into a new technology, the genetic modification of food, and they were actually asking the government to oversee their emerging industry. But this was late 1986. Ronald Reagan was president and the administration was busily deregulating business. Bush needed convincing. “We bugged him for regulation,” said Leonard Guarraia, one of the executives at the meeting. “We told him that we have to be regulated.”[1] Monsanto was about to make a multibillion-dollar gamble. With this new technology, they could engineer and patent a whole new kind of food. Later, by buying up seed companies around the world, Monsanto could replace the natural seeds with their patented engineered seeds and control a hefty portion of the food supply. But there was fear among Monsanto’s ranks—fear of consumers’ and environmentalists’ reactions. Their fear was borne of experience. Years earlier, Monsanto had assured the public that their Agent Orange, the defoliant used during the Vietnam War, was safe for humans. It wasn’t. Thousands of veterans and tens of thousand of Vietnamese who suffered a wide range of maladies, including cancer, neurological disorders, and birth defects, blame Monsanto.

Genetic atomism is dead. Hereditary stability and hereditary change are both based, not on a mosaic of genes, but on the action of the gene-complex 'as a whole'. But this face-saving expression-which is now coming into increased use-is empty, like so many other holistic formulations, unless we interpolate between the gene-complex as a whole, and the individual gene, a hierarchy of genetic sub-assemblies-self-regulating holons of heredity, which control the development of organs, and also control their possible evolutionary modifications, by canalising the effects of random mutations. A hierarchy with its built-in, self-regulatory safeguards is a stable affair. It cannot be pulled in here, pulled out there, like Patou belabouring his model. It is capable of variation and change, but only in co-ordinated ways and only in limited directions.

A note of caution: epigenetics is also on the verge of transforming into a dangerous idea. Epigenetic modifications of genes can potentially superpose historical and environmental information on cells and genomes—but this capacity is speculative, limited, idiosyncratic, and unpredictable: a parent with an experience of starvation produces children with obesity and overnourishment, while a father with the experience of tuberculosis, say, does not produce a child with an altered response to tuberculosis. Most epigenetic “memories” are the consequence of ancient evolutionary pathways, and cannot be confused with our longing to affix desirable legacies on our children. As with genetics in the early twentieth century, epigenetics is now being used to justify junk science and enforce stifling definitions of normalcy. Diets, exposures, memories, and therapies that purport to alter heredity are eerily reminiscent of Lysenko’s attempt to “reeducate” wheat using shock therapy. Mothers are being asked to minimize anxiety during their pregnancy—lest they taint all their children, and their children, with traumatized mitochondria. Lamarck is being rehabilitated into the new Mendel. These glib notions about epigenetics should invite skepticism. Environmental information can certainly be etched on the genome. But most of these imprints are recorded as “genetic memories” in the cells and genomes of individual organisms—not carried forward across generations. A man who loses a leg in an accident bears the imprint of that accident in his cells, wounds, and scars—but does not bear children with shortened legs. Nor has the uprooted life of my family seem to have burdened me, or my children, with any wrenching sense of estrangement. Despite Menelaus’s admonitions, the blood of our fathers is lost in us—and so, fortunately, are their foibles and sins. It is an arrangement that we should celebrate more than rue. Genomes and epigenomes exist to record and transmit likeness, legacy, memory, and history across cells and generations. Mutations, the reassortment of genes, and the erasure of memories counterbalance these forces, enabling unlikeness, variation, monstrosity, genius, and reinvention—and the refulgent possibility of new beginnings, generation upon generation.

I described living cells as being crammed full of protein molecules. Acting individually or in small assemblies, they perform reiterated molecular processes that can be regarded, I argued, as a form of computation. Moreover, large numbers of proteins linked into huge interacting networks operate, in effect, like circuits of electrical or electronic devices. Networks of this kind are the basis for the animate wanderings of single cells and their ability to choose what to do next. Here I have broadened the view to encompass multiple cells - 'societies' of cells. Through a variety of strategies - including diffusive hormones, electrical signals, and mechanical interactions - the computational networks of individual cells are linked. During evolution, cells acquired the capacity to work together in social groups; it became advantageous for most cells to become highly specialised. Liver cells, muscle cells, skin cells, and so on abandoned their opportunities for unlimited replication. They began the communal expansion of interlinked abilities that led to the plants and animals we see around us today. But the basis of this diversification of cell chemistry was yet another form of computation - one that operates on DNA. Control mechanisms, again based on protein switches, created extensive but subtle modifications of the core genetic information.

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What holds cells in this teetering position? In 2006, a group headed by Eric Lander at the Broad Institute in Boston, found at least part of the answer. A key set of genes in ES cells, the pluripotent cells we have come to know so well, were found to have a really strange histone modification pattern. These were genes that were very important for controlling if an ES cell stayed pluripotent, or differentiated. Histone H3K4 was methylated at these genes, which normally is associated with switching on gene expression. H3K27 was also methylated. This is normally associated with switching off gene expression. So, which modification would turn out to be stronger? Would the genes be switched on or off? The answer turned out to be both. Or neither, depending on which way we look at it. These genes were in a state called ‘poised’. Given the slightest encouragement – a change in culture conditions that pushed cells towards differentiation for example – one or other of these methylations was lost. The gene was fully switched on, or strongly repressed, depending on the epigenetic modification

There is increasing evidence that at least some of the targeting of epigenetic modifications can be explained by interactions with long ncRNAs. Jeannie Lee and her colleagues have recently investigated long ncRNAs that bind to a complex of proteins. The complex is called PRC2 and it generates repressive modifications on histones. PRC2 contains a number of proteins, and the one that interacts with the long ncRNAs is probably EZH2. The researchers found that the PRC2 complex bound to literally thousands of different long ncRNA molecules in embryonic stem cells from mice13. These long ncRNAs may act as bait. They can stay tethered to the specific region of the genome where they are produced, and then attract repressive enzymes to shut off gene expression. This happens because the repressive enzyme complexes contain proteins like EZH2 that are capable of binding to RNA.

The Air ncRNA gave scientists important insights into how these long ncRNAs repress gene expression. The ncRNA remained localised to a specific region in the cluster of imprinted genes, and acted as a magnet for an epigenetic enzyme called G9a. G9a puts a repressive mark on the histone H3 proteins in the nucleosomes deposited on this region of DNA. This histone modification creates a repressive chromatin environment, which switches off the genes.

However, other than the miraculous modifications achieved in nature millennia ago, not a single acre of genetically modified wheat is grown for commercial purposes anywhere in the world.

In this model, there is a vicious cycle of events that results in the generation of a more and more repressed state. One of the predictions from this model is that repressive histone modifications attract DNA methyltransferases, which deposit DNA methylation near those histones. This methylation in turn attracts more repressive histone modifying enzymes, creating a self-perpetuating cycle that leads to an increasingly hostile region for gene expression. Experimental data suggest that in many cases this model seems to be right. Repressive histone modifications can act as the bait to attract DNA methylation to the promoter of a tumour suppressor gene. A key example of this is an epigenetic enzyme we met in the previous chapter, called EZH2. The EZH2 protein adds methyl groups to the lysine amino acid at position 27 on histone H3. This amino acid is known as H3K27. K is the single letter code for lysine (L is the code for a different amino acid called leucine).

He has shown that these poised histone modifications are found in early cancer stem cells and are really significant for setting the DNA methylation patterns in cancer cells

It’s abundantly clear that these events do happen, and quite frequently, but often it’s been difficult to identify exactly how a tumour suppressor has mutated. In the last fifteen years, we’ve started to realise that there is another way that a tumour suppressor gene can become inactivated. The gene may be silenced epigenetically. If the DNA at the promoter becomes excessively methylated or the histones are covered in repressive modifications, the tumour suppressor will be switched off. The gene has been inactivated without changing the underlying blueprint.

In our model, treatment with 5-azacytidine will drive down the DNA methylation for as long as the patients take the drug. Unfortunately, many cancer drugs have serious side-effects and the DNMT inhibitors are no exception. The side effects may eventually become such a problem that the patient has to stop taking the drug. However, the patient’s cancer cells probably still have histone modifications at the tumour suppressor genes. Once the patient stops taking 5-azacytidine, these histone modifications almost certainly start to attract the DNMT enzymes all over again, re-initiating stable repression of gene expression.

Part of this may involve the small percentage of histones that are present in the sperm genome. Many of these are located at the imprinting control regions, and may protect these regions from reprogramming when the sperm and the egg fuse25. Histone modifications also play a role in establishing ‘new’ imprints during gamete production. It seems to be important that the imprinting control regions lose any histone modifications that are associated with switching genes on. Only then can the permanent DNA methylation be added26. It’s this permanent DNA methylation that marks a gene with a repressive imprint.

There’s an amazing family of genes, called HOX genes. When they’re mutated in fruit flies (Drosophila melanogaster) the results are incredible phenotypes, such as legs growing out of the head14. There’s a long ncRNA known as HOTAIR, which regulates a region of genes called the HOX-D cluster. Just like the long ncRNAs investigated by Jeannie Lee, HOTAIR binds the PRC2 complex and creates a chromatin region which is marked with repressive histone modifications. But HOTAIR is not transcribed from the HOX-D position on chromosome 12. Instead it is encoded at a different cluster of genes called HOX-C on chromosome 215. No-one knows how or why HOTAIR binds at the HOX-D position. There’s a related mystery around the best studied of all long ncRNAs, Xist. Xist ncRNA spreads out along almost the entire inactive X chromosome but we really don’t know how. Chromosomes don’t normally become smothered with RNA molecules. There’s no obvious reason why Xist RNA should be able to bind like this, but we know it’s nothing to do with the sequence of the chromosome. The experiments described in the last chapter, where Xist could inactivate an entire autosome as long as it contained an X inactivation centre, showed that Xist just keeps on travelling once it’s on a chromosome. Scientists are basically still completely baffled about these fundamental characteristics of this best-studied of all ncRNAs.

All the reprogramming of the genome in early development has multiple effects. It allows two highly differentiated cell types to fuse and form one pluripotent cell. It balances out the competing demands of the maternal and paternal genomes, and ensures that this balancing act can be re-established in every generation. Reprogramming also prevents inappropriate epigenetic modifications being passed from parent to offspring. This means that even if cells have accumulated potentially dangerous epigenetic changes, these will be removed before they are passed on. This is why we don’t normally inherit acquired characteristics. But there are certain regions of the genome, such as IAP retrotransposons, that are relatively resistant to reprogramming. If we want to work out how certain acquired characteristics – responses to vinclozolin or responses to paternal nutrition, for example – get transmitted from parent to offspring, these IAP retrotransposons might be a good place to start looking.

Reprogramming is what John Gurdon demonstrated in his ground-breaking work when he transferred the nuclei from adult toads into toad eggs. It’s what happened when Keith Campbell and Ian Wilmut cloned Dolly the Sheep by putting the nucleus from a mammary gland cell into an egg. It’s what Yamanaka achieved when he treated somatic cells with four key genes, all of which code for proteins highly expressed naturally during this reprogramming phase. The egg is a wonderful thing, honed through hundreds of millions of years of evolution to be extraordinarily effective at generating vast quantities of epigenetic change, across billions of base-pairs. None of the artificial means of reprogramming cells comes close to the natural process in terms of speed or efficiency. But the egg probably doesn’t quite do everything unaided. At the very least, the pattern of epigenetic modifications in sperm is one that allows the male pronucleus to be reprogrammed relatively easily. The sperm epigenome is primed to be reprogrammed6. Unfortunately, these priming chromatin modifications (and many other features of the sperm nucleus), are missing if an adult nucleus is reprogrammed by transferring it into a fertilised egg. That’s also true when an adult nucleus is reprogrammed by treating it with the four Yamanaka factors to create iPS cells. In both these circumstances, it’s a real challenge to completely reset the epigenome of the adult nucleus. It’s just too big a task. This is probably why so many cloned animals have abnormalities and shortened lifespans. The defects that are seen in these cloned animals are another demonstration that if early epigenetic modifications go wrong, they may stay wrong for life. The abnormal epigenetic modification patterns result in permanently inappropriate gene expression, and long-term ill-health.

All this reprogramming of the genome in normal early development changes the epigenome of the gametes and creates the new epigenome of the zygote. This ensures that the gene expression patterns of eggs and sperm are replaced by the gene expression patterns of the zygote and the subsequent developmental stages. But this reprogramming also has another effect. Cells can accumulate inappropriate or abnormal epigenetic modifications at various genes. These disrupt normal gene expression and can even contribute to disease, as we shall see later in this book. The reprogramming of the egg and the sperm prevent them from passing on from parent to offspring any inappropriate epigenetic modifications they have accumulated. Not so much wiping the slate clean, more like re-installing the operating system.

Even though these individuals had seemed perfectly healthy at birth, something that had happened during their development in the womb affected them for decades afterwards. And it wasn’t just the fact that something had happened that mattered, it was when it happened. Events that take place in the first three months of development, a stage when the foetus is really very small, can affect an individual for the rest of their life. This is completely consistent with the model of developmental programming, and the epigenetic basis to this. In the early stages of pregnancy, where different cell types are developing, epigenetic proteins are probably vital for stabilising gene expression patterns. But remember that our cells contain thousands of genes, spread over billions of base-pairs, and we have hundreds of epigenetic proteins. Even in normal development there are likely to be slight variations in the expression of some of these proteins, and the precise effects that they have at specific chromosomal regions. A little bit more DNA methylation here, a little bit less there. The epigenetic machinery reinforces and then maintains particular patterns of modifications, thus creating the levels of gene expression. Consequently, these initial small fluctuations in histone and DNA modifications may eventually become ‘set’ and get transmitted to daughter cells, or be maintained in long-lived cells such as neurons, that can last for decades. Because the epigenome gets ‘stuck’, so too may the patterns of gene expression in certain chromosomal regions. In the short term the consequences of this may be relatively minor. But over decades all these mild abnormalities in gene expression, resulting from a slightly inappropriate set of chromatin modifications, may lead to a gradually increasing functional impairment. Clinically, we don’t recognise this until it passes some invisible threshold and the patient begins to show symptoms.

Here’s the sequence of epigenetic events in very early development: The male and female pronuclei (from the sperm and the egg respectively) are carrying epigenetic modifications; The epigenetic modifications get taken off (in the immediate post-fertilisation zygote); New epigenetic modifications get put on (as the cells begin to specialise). This is a bit of a simplification. It’s certainly true that researchers can detect huge swathes of DNA demethylation during stage 2 from this list. However, it’s actually more complicated than this, particularly in respect of histone modifications. Whilst some histone modifications are being removed, others are becoming established. At the same time as the repressive DNA methylation is removed, certain histone marks which repress gene expression are also erased. Other histone modifications which increase gene expression may take their place. It’s therefore too naïve to refer to the epigenetic changes as just being about putting on or taking off epigenetic modifications. In reality, the epigenome is being reprogrammed.

Pacalet is a well-known figure in the natural wine scene, but, like many in this unofficial club, he’s not easy to compartmentalize. He believes in natural fermentation without the addition of SO2 or yeasts, but he doesn’t care for biodynamics or organics. “It’s very easy to pay and become organic, not really taking any risks,” he says. “But to make natural wine, you do have to take risks.” Pacalet thinks that the current vine material is weak because of continued asexual reproduction. “The vines are in a degenerate state,” he maintains. “Maybe we can use OGM [genetic modification] in the right way, in the hands of good people, to help here.” Pacalet uses whole bunches in his Pinot Noir fermentations, and he maintains that the stems help capture some of the heat from fermentation. He hasn’t had to regulate temperature for ten years and says that different terroirs ferment at different temperatures. This view accords with the terroir concept at the heart of natural wine. Pacalet is slightly unusual among natural wine producers in that he is working in a prestigious region; many work in less fashionable regions, such as the various appellations in the Loire or in Beaujolais.

April 2015, China announced its use of a new technology known as CRISPR (Clustered Regularly Interspersed Palindromic Repeats), used for the purpose of simplified gene editing. This new genetic modification technology is fast, simple to use, and inexpensive. A recent Chinese biotech start-up named Amino has brought this technology to everyone in a kit that retails for just under seven hundred dollars. Yes, for less than a good smartphone,

Look at them, the bugs. Humans have used everything in their power to extinguish them: every kind of poison, aerial sprays, introducing and cultivating their natural predators, searching for and destroying their eggs, using genetic modification to sterilize them, burning with fire, drowning with water. Every family has bug spray, every desk has a flyswatter under it . . . this long war has been going on for the enitre history of human civilization. But the outcome is still in doubt. The bugs have not been eliminated. They still proudly live between the heavens and the earth, and their numbers have not been diminished from the time before the appearance of the humans. The Trisolarans who deemed the humans bugs seemed to have forgotten one fact: The bugs have never been truly defeated. A small black cloud covered the sun and cast a moving shadow against the ground. This was not a common cloud, but a swarm of locusts that had just arrived. As the swarm landed in the fields nearby, the three men stood in the middle of a living shower, feeling the dignity of life on Earth. Ding yi and Wang Miao poured the two bottles of wine they had with them on the gorund beneath their feet, a toast for the bugs.

Continuing to do research on genetic modification, and occasionally using successfully modified organisms for specific purposes such as the production of expensive drugs, make good sense. Helping developing countries to produce more food is a worthy aim, but it is sometimes used as an excuse for an alternative agenda, or as a convenient way to demonise opponents. There is little doubt that the technology needs better regulation: I find it bizarre that standard food safety tests are not required, on the grounds that the plants have not been changed in any significant way, but that the innovations are so great that they deserve patent protection, contrary to the long-standing view that naturally occurring objects and substances cannot be patented. Either it’s new, and needs testing like anything else, or it’s not, and should not be patentable. It is also disturbing, in an age when commercial sponsors blazon their logos across athletes’ shirts and television screens, that the biotechnology industry has fought a lengthy political campaign to prevent any mention of their product being placed on food. The reason is clear enough: to avoid any danger of a consumer boycott. But consumers are effectively being force-fed products that they may not want, and whose presence is being concealed. Our current understanding of genetics and ecology is inadequate when it comes to the widespread use of genetically modified organisms in the natural environment or agriculture. Why take the risk of distributing the material, when the likely gains for most of us – as opposed to short-term profits for biotechnology companies – are tiny or non-existent?

The ‘epi’ in epigenetics is derived from Greek and means at, on, to, upon, over or beside. The DNA in our cells is not some pure, unadulterated molecule. Small chemical groups can be added at specific regions of DNA. Our DNA is also smothered in special proteins. These proteins can themselves be covered with additional small chemicals. None of these molecular amendments changes the underlying genetic code. But adding these chemical groups to the DNA, or to the associated proteins, or removing them, changes the expression of nearby genes. These changes in gene expression alter the functions of cells, and the very nature of the cells themselves. Sometimes, if these patterns of chemical modifications are put on or taken off at a critical period in development, the pattern can be set for the rest of our lives,

In the same way that Firestone’s embrace of scientific and technological progress as manifest destiny tips its hat to Marx and Engels, so also it resembles (perhaps even more closely) the Marxist-inspired biofuturism of the interwar period, particularly in Britain, in the work of writers such as H. G. Wells, J. B. S. Haldane, J. D. Bernal, Julian Huxley, Conrad Waddington, and their contemporaries (including Gregory Bateson and Joseph Needham, the latter of whose embryological interests led to his enduring fascination with the history of technology in China). Interestingly, it is also in these early twentieth century writings that ideas about artificial reproduction, cybernation, space travel, genetic modification, and ectogenesis abound. As cultural theorist Susan Squier has demonstrated, debates about ectogenesis were crucial to both the scientific ambitions and futuristic narratives of many of the United Kingdom’s most eminent biologists from the 1920s and the 1930s onward. As John Burdon Sanderson (“Jack”) Haldane speculated in his famous 1923 paper “Daedalus, or Science and the Future” (originally read to the Heretics society in Cambridge) ectogenesis could provide a more efficient and rational basis for human reproduction in the future: [W]e can take an ovary from a woman, and keep it growing in a suitable fluid for as long as twenty years, producing a fresh ovum each month, of which 90 per cent can be fertilized, and the embryos grown successfully for nine months, and then brought out into the air.

it’s possible, through lifestyle change, to change how our DNA expresses itself. These modifications can influence how cells divide and what proteins are made, and even what genetic material is passed on to our offspring.

He got what he wanted. He’s a billionaire with a genetic modification process he wouldn’t have without Elaine. He’s not even supposed to remember any of us.

Therefore, we must invest in research that allows us to grow more healthy food and transport it more effectively. And please make no mistake: that includes accepting genetically modified crops, those engineered to include a trait in the plant that doesn’t occur in its wild form, such as resistance to insects, tolerance to drought, greater vitamin A production, or more efficient use of sunlight to convert CO2 to sugar—as an absolutely necessary part of our food future. With more efficient plants, we could feed up to 200 million additional people, just from plants grown in the US Midwest. 33 These crops have gotten a bad rap for being “unnatural,” although many people who hold this view don’t recognize that most of the food we think of as “natural” has already been subject to significant genetic manipulation. The ears of corn you see at the grocery store look nothing like the wild plant from which modern corn came; over the course of nine thousand years, the spindly finger-length grass known as teosinte was cultivated to evolve larger cobs and more rows of plump, soft, sugary kernels, a process of modification that significantly altered the plant’s genome.34 The apples we’ve grown accustomed to eating have a bit more resemblance to their small, wild ancestors, but good luck finding one of those ancestors; they have been nearly wiped off the planet, and that’s no great loss to our diet, since the biggest genetic contributor to modern apples, Malus sylvestris, is so tart it’s darn near inedible.

Conversely, animals can be quite sensitive to human music. There are stories of dogs who hide under the couch for piano works by atonal composers but not for those by, say, Mozart. One music teacher told me that her dog would heave an audible sigh of relief if she stopped playing complex, fast-moving pieces by Franz Liszt and proceeded to something calmer. And there are reports of cows that produce more milk listening to Beethoven (although, if this is true, shouldn't one hear more classical music on farms?). Birds listen as carefully to sounds as any musician. They have to, because they learn from each other. Many birds are not born with the song they sing: the symphonies they offer us for free in forests and meadows are cultural. White-crowned sparrows, for example, develop their normal song only when they have been exposed early in life to the sounds of an adult of their species. Many songbirds have dialects-differences in song structure from one population to another. One theory about this is that if a female can tell from a male's song that he is a local boy, she may prefer him as a mate, as he may be genetically adapted to regional conditions. Given the variability in song from location to location it is hard to maintain that birdsong is instinctive in the usual sense. There is room for creativity and modification. Some individuals act as star performers, setting new trends in their region.

Given that the modification is so small, it’s perhaps surprising that it will come up over and over again in this book, and in any discussion of epigenetics. This is because methylation of DNA has profound effects on how genes are expressed, and ultimately on cellular, tissue and whole-body functions.

The proposition that business firms are entitled to patent protection when they have produced variations in the genetic structure of plants (GMOs) conveniently ignores the fact that the pre-existing plants had, themselves, arisen from modifications or adaptations provided by our ancient ancestors.

Genetic modification” refers to several techniques for changing organisms to suit our wants and needs. The technology involves various methods for inserting one or more specific genes directly into a target organism, or selectively altering or silencing a gene that is already there. There are two basic types of gene insertions: transgenic and cisgenic. Cisgenic insertion involves inserting genes from closely related species, ones that could potentially crossbreed with the target species. Transgenic insertion involves genes from distant species—even from different kingdoms of life, such as putting a gene from a bacterium into a plant.

The genetic mechanisms that were described here are a collection of exotic mutations: new cis-regulatory elements from transposable elements; novel transcription factor functions; and new miRNAs. It seems that rewiring a gene regulatory network, as required for the evolution a morphological novelty, uses a quite different set of mechanisms than usually associated with adaptive changes that is, changes in enzyme activity and gene expression due to small changes in cis-regulatory elements. This distinction hints at the possibility that the difference between adaptation and innovation is not only conceptual, but that the conceptual difference might be mirrored by a difference in the molecular mechanisms. It is far from clear whether this distinction will hold up, because there are still only a limited number of cases of innovations that are understood at the molecular level. However, one should at not prematurely dismiss this possibility. The possibility of a mechanistic difference beween adaptation and innovation is also interesting because the characteristics of the genetic mechanisms may explain the phenomenology of innovations; innovations tend to be rare and episodic and result in a phenotype that tends to be canalized in its major features. As discussed above, one of the main characteristics of mutations by transposable elements is that they are episodic and specific to certain lineages. Mutations caused by transposable elements are most prevalent after the infection of a genome by a new retrovirus or any other new transposable elements. Similarly, gene duplications also temporarily open a window of evolvability by releasing constraints on gene evolution, and the maintenance of duplicated genes is often associated with body plan innovations. There is also a tendency for maintaining novel genetic elements with the origin of morphological novelties: new genes, new cis-regulatory elements, new miRNAs, and probably many others. Transcription factor protein evolution is likely necessary for the evolution of novel functional specificities, and miRNAs are involved in canalizing phenotypes once they have arisen. Hence, the conceptual uniqueness of innovations (i.e., the origination of novel cell type or of a quasi-independent body part) as compared to adaptation (i.e. the modification of existing body parts and physiological processes) may require a set of mutational mechanisms that can radically rewire gene regulatory networks and stabilize/canalize the phenotypic product of these changes. If further research supports this idea, then the conceptual distinction between adaptation and innovation will be linked to and grounded in the distinctness of the underlying molecular mechanisms.