Tag Archives: natural selection

Darwin’s finches highlight the unity of all life

The Conversation

Frank Nicholas, University of Sydney

When Charles Darwin visited the Galapagos Islands in October 1835, he and his ship-mates on board HMS Beagle collected specimens of birds, including finches and mockingbirds, from various islands of the archipelago.

At the time, Darwin took little interest in the quaint finches, making only a one-word mention of them in his diary. As painstakingly shown by Frank Sulloway and more recently by John Van Whye, it wasn’t until two years later that the finches sparked Darwin’s interest.

By then he had received feedback from the leading taxonomist of the time, John Gould, that the samples comprised 14 distinct species, none of which had been previously described! Gould also noted that their “principal peculiarity consisted in the bill [i.e. beak] presenting several distinct modifications of form”.

So intrigued was Darwin by this variation in size and shape of beaks that in the second (1845) edition of Journal of Researches he included illustrations of the distinctive variation between species in the size and shape of their beaks. He added a comment that:

Seeing this gradation and diversity of structure in one small, intimately related group of birds, one might really fancy that from an original paucity of birds in this archipelago, one species had been taken and modified for different ends.

The famously varied beak shapes of the Galapagos finches, as illustrated in the second edition of Darwin’s Journal of Researches.
Wikimedia

Unfortunately for Darwin, the closer he examined the available evidence on Galapagos finches, the more confusing the picture became. This was partly because the specimens available to him were not sufficiently labelled as to their island of collection.

Presumably, it was his doubt about the available evidence that resulted in Darwin making no mention of Galapagos finches in any edition of Origin of Species.

Why, then, do people now label them as “Darwin’s finches”, and why are these finches now regarded as a classical textbook example of his theory of evolution by natural selection?

Paragons of evolution

Despite not mentioning Galapagos finches, Darwin did make much use of evidence from other Galapagos species (especially mockingbirds) in Origin of Species.

As the influence of Origin of Species spread, so too did the evolutionary fame of the Galapagos Islands. Increasingly, other biologists were drawn into resolving the questions about finches that Darwin had left unanswered.

By the end of the 19th century, Galapagos finches were among the most studied of all birds. By the mid-20th century, there was abundant evidence that Galapagos finches had evolved to fill the range of ecological niches available in the archipelago – a classic example of evolution by adaptive radiation.

Beak size and shape were key attributes in determining adaptation to the different types of food available. In the second half of the 20th century, classic research by Princeton University’s Peter and Rosemary Grant provided evidence of quite strong natural selection on beak size and shape.

Under the hood

New light has also been shed on the evolution of Darwin’s finches in a paper recently published in Nature. In this latest research, the entire genomes of 120 individual birds from all Galapagos species plus two closely related species from other genera were sequenced.

The work was done by a team led by Swedish geneticist Leif Andersson, with major input from Peter and Rosemary Grant, who are still leading experts on the finches.

Comparison of sequence data enabled them to construct a comprehensive evolutionary tree based on variation across the entire finch genome. This has resulted in a revised taxonomy, increasing the number of species to 18.

The most striking feature of the genome-based tree is the evidence for matings between different populations, resulting in the occasional joining of two branches of the tree. This evidence of “horizontal” gene flow is consistent with field data on matings of finches gathered by the Grants.

A comparison of whole-genome sequence between two closely related groups of finches with contrasting beak shape (blunt versus pointed) identified at least 15 regions of chromosomes where the groups differ substantially in sequence.

Unity of life

The most striking difference between the two groups was observed in a chromosomal region containing a regulatory gene called ALX1. This gene encodes a polypeptide that switches other genes on and off by binding to their regulatory sequences.

Like other such genes, ALX1 is crucially involved in embryonic development. Indeed, mutations in ALX1 in humans and mice give rise to abnormal development of the head and face.

It is an extraordinary illustration of the underlying unity of all life on Earth that Leif Andersson and his colleagues have shown that the ALX1 gene also has a major effect on beak shape in finches, and that this gene has been subject to natural selection during the evolution of the Galapagos finches.

If Darwin were alive today, he would be astounded at the power of genomics tools such as those used in generating the results described in this paper. He would also be delighted to see such strong evidence not only in support of evolution but also in support of one of its major forces, natural selection.

The ConversationFrank Nicholas is Emeritus Professor of Animal Genetics at University of Sydney

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

 

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Darwin’s theory may be brilliant but it doesn’t explain everything

The Conversation

Lewis Dean, University of St Andrews and Kate Cross, University of St Andrews

As evolutionary scientists, we devote much of our working lives to exploring the behaviour of humans and other animals through an evolutionary lens. So it may come as a surprise that our show at this year’s Edinburgh Fringe is named Alas, Poor Darwin …?, borrowing from one of the most searing critiques of evolutionary psychology ever written. We’ve added a question mark, but still – it’s no simple tale of how our minds evolved.

Evolutionary theory is a bit like a chocolate ice cream in the hands of a two-year old: it’s going to get applied everywhere, but will anything useful be achieved in the process? The central tenets of Darwinian theory – variability, heredity and selection – are as beautiful as they are compelling. They completely revolutionised biology.

But applying these principles to the study of human behaviour has caused far more controversy. The evolutionary explanations for human behaviour that grab the headlines can often be neat; really neat – like tightly-plotted narratives in which everything works out perfectly in the end, usually with a guy getting a girl, where everything happens for a reason.

Real life rarely makes for such a neat story. We’ve all seen enough action movies to notice that the more satisfying the ending, the more plot holes you have to ignore as you walk out of the cinema. Neatness makes a good story, but it’s not enough for good science.

Ovulation meets evolution

One good example of this problem is the story of how women’s preferences for masculine male partners shift throughout the menstrual cycle in a strategic way. It goes like this: at the time of ovulation, when “good genes” are most important, women are attracted to more masculine men. For the rest of the menstrual cycle when faithfulness and cooperation are paramount, the opposite is true (we’re glossing over some subtleties that are explained here).

‘Don’t blame me’ Everett Historical

In a similar vein, there’s an elegant account of male violence. It says that men are more likely than women to behave aggressively everywhere in the world because in the Pleistocene epoch (between 10,000 and 1.7m years ago), humans had a polygynous mating system, meaning one man mating with several women. The men who succeeded in aggressive competition with other men had more partners, and therefore more children, and so more of their genes got passed on.

These stories prompt some awkward questions. For example does a change in women’s attraction have to be directly selected for? Could it be the by-product of some other evolutionary process? Can we be sure that the preferences reported in the lab by female undergraduates in 2015 are a good proxy for the real-life choices made by women 100,000 years ago? What evidence is there that our ancestors were polygynous? What selection pressures were acting on women while the men were all busy fighting? (Women’s genes also get passed on to their children, in case anyone had forgotten.)

You begin to find that very accomplished scientists who know an awful lot about evolution and human behaviour disagree. Vociferously. And there’s a good reason for this: they’re scientists. Destruction-testing of ideas is very much in the job spec.

The reality of scientific enquiry

In our own work we don’t generally find neat, satisfying stories that are easy to tell, hard to critique, and make everything fall into place. We tend to end up with tantalising hypotheses, really interesting ideas that might be true but we haven’t quite gathered the data to nail down beyond all doubt. We find theories that are dazzling in their elegance but multitudinous in their caveats.

We find that the mind steadfastly refuses to behave like a collection of perfectly adapted units, each with a single function that afforded a clear evolutionary advantage at some weirdly specific yet curiously under-specified time during human evolutionary history. Instead the human mind seems to be full of compromises and by-products, highly flexible, and intricately intertwined with this weird thing called “human culture”.

Yet having been drawn to evolutionary science for its extraordinary elegance and having found a thousand times more questions than satisfactory answers, we persist. Because if you expand your ideas about what “evolutionary” means – if you cease looking for the neat stories and embrace the fact that it’s going to get very, very messy, you can start to get somewhere really interesting.

Culture and evolution are not opposites. Evolved doesn’t have to mean adaptation. It might or might not mean “useful under some circumstances”. (It certainly doesn’t mean – and has never meant – good or right).

Refuting one evolutionary hypothesis about human behaviour doesn’t invalidate all of them. That would be like saying that evolutionary theory is felled by the old question, “But if we evolved from monkeys, why are there still monkeys?”

Arguing about the how, when and why isn’t a sign of science denialism, nor a reason to scrap the whole line of investigation – it’s healthy disagreement and we’d like to see more of it. Being an evolutionary scientist is a bit like being Dirk Gently: you might not get where you were hoping to go, but you’ll probably end up somewhere it’s worth being.

Kate and Lewis’s show, Alas Poor Darwin …?, part of the Cabaret of Dangerous Ideas, is taking place at the Edinburgh Fringe on August 16

The ConversationLewis Dean is Research Fellow at University of St Andrews and Kate Cross is Lecturer in Psychology at University of St Andrews

This article was originally published on The Conversation. (Reblogged by permission). Read the original article.

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Charles Darwin – where he was right and wrong

by Tim Harding, B.Sc.

(An edited version of this essay was published in The Skeptic magazine, June 2015, Vol 35 No 2, under the title ‘Darwin’s Missing Link’.  The essay is based on a talk presented to the Mordi Skeptics on Tuesday 5 May 2015).

Charles Darwin (1809-1882) is best known for his major contributions to evolutionary theory. In 1859, Darwin published his theory of natural selection as the mechanism of evolution in his revolutionary book On the Origin of Species. This book provided compelling evidence overcoming the scientific rejection of earlier concepts of transmutation of species. The basic principles of his theory have been shown to be correct and are now widely accepted as the basis of mainstream zoology, botany and ecology.

On the other hand, in a later book Darwin got it wrong with the mechanisms of inheritance.  The empirical rules of genetics, based solely on observational results, were largely understood since Gregor Mendel’s ‘wrinkled pea’ experiments in the 1860s. The postulated units of inheritance were called genes, but in Charles Darwin’s time it was not understood where genes were located in the body or what they physically consisted of. Darwin knew that there must have been a physical mechanism for inheritance, but his speculations about it – called pangenesis – were incorrect. Fortunately for the credibility of his theory of evolution by natural selection, he published these speculations later in a separate 1868 book titled Variation of Animals and Plants Under Domestication.

Darwin’s early career

Charles Robert Darwin was born in Shrewsbury, England, on 12 February 1809 at his family home, The Mount. He was the fifth of six children of wealthy society doctor and financier Robert Darwin, and Susannah Darwin (née Wedgwood).

Darwin went to Edinburgh University in 1825 to study medicine. In his second year he neglected his medical studies for natural history and spent four months assisting Robert Grant’s research into marine invertebrates. Grant revealed his enthusiasm for the concept of transmutation of species (the altering of one species into another), but Darwin initially rejected this concept (probably for religious reasons).

Ideas about the transmutation of species were controversial as they conflicted with theological beliefs that species were unchanging parts of a designed hierarchy and that humans were unique, unrelated to other animals. The political and religious implications were intensely debated, but transmutation was not accepted by the scientific mainstream until Darwin’s theory.

In December 1831, Darwin had joined the Beagle ship voyage as a gentleman naturalist and geologist.  In South America, he discovered fossils resembling huge armadillos, and noted the geographical distribution of modern species in hope of finding their ‘centre of creation’.  As the Beagle neared England in 1836, he began to think that species might not be immutable after all.

In March 1837, ornithologist John Gould announced that mockingbirds collected on the Galápagos Islands represented three separate species each unique to a particular island, and that several distinct birds from those islands were all classified as finches. Darwin began speculating, in a series of notebooks, on the possibility that ‘one species does change into another’ to explain these findings, and around July of that year sketched a genealogical branching of a single evolutionary tree.  Unconventionally, Darwin asked questions of fancy pigeon and animal breeders as well as established scientists.

Charles Darwin

Charles Darwin in 1860, aged 51

In late September 1838, Darwin started reading Thomas Malthus’s An Essay on the Principle of Population with its statistical argument that human populations, if unrestrained, breed beyond their means and struggle to survive. Darwin related this to the struggle for existence among wildlife and plants, so that the survivors would pass on their form and abilities, and unfavourable variations would be destroyed.  By December 1838, he had noted a similarity between the act of breeders selecting traits and a Malthusian nature selecting among variants thrown up by chance.

Darwin now had the framework of his theory of natural selection, but he was fully occupied with his career as a geologist and held off writing a sketch of his theory until his book on The Structure and Distribution of Coral Reefs was completed in May 1842.

Evolution by natural selection

Darwin continued to research and extensively revise his theory of natural selection while focusing on his main work of publishing the scientific results of the Beagle voyage.  He tentatively wrote of his ideas to the famous Scottish geologist Charles Lyell in January 1842; then in June he roughed out a 35-page pencil sketch of his theory. Darwin began correspondence about his theorising with the botanist Joseph Dalton Hooker in January 1844, and by July had rounded out his sketch into a 230-page essay, to be expanded with his research results and published if he died prematurely.

His famous 1859 book On the Origin of Species was written for non-specialist readers and attracted widespread interest upon its publication. As Darwin was already an eminent scientist, his findings were taken seriously.  The evidence he presented generated scientific, philosophical, and religious discussion. The debate over the book contributed to the campaign by Thomas Huxley and his fellow members of the X Club to secularise science by promoting scientific naturalism. Within two decades there was widespread scientific agreement that evolution, with a branching pattern of common descent, had occurred, but scientists were slow to give the mechanism of natural selection the significance that it deserved.

species divergence

Diagram representing the divergence of species, from Darwin’s Origin of Species

Darwin’s theory of evolution is based on some key facts (based on wild populations without human interference), which biologist Ernst Mayr has summarised as follows:

  • Every species is fertile enough that if all offspring survived to reproduce the population would grow.
  • Despite periodic fluctuations, populations remain roughly the same size.
  • Resources such as food are limited and are relatively stable over time.
  • Individuals in a population vary significantly from one another.
  • Much of this variation is heritable.

From these key facts, the following important inferences may be made, once again summarised by Ernst May:

  • A struggle for survival ensues.
  • Individuals less suited to the environment are less likely to survive and less likely to reproduce.
  • Individuals more suited to the environment are more likely to survive and more likely to reproduce and leave their heritable traits to future generations, which produces the process of natural selection.
  • This slow process gradually results in populations changing to adapt to their environments, and ultimately, these variations accumulate over time to form new species.

Natural selection provided a mechanism for variation and eventual speciation, but it did not explain the inheritance of variation.  Without some way to explain the inheritance of characteristics acted on by natural selection, his theory would be incomplete.

Mechanisms of inheritance

Before the advent of genetics, Hippokratic theories attempted to explain inheritance in terms of a blending of fluids extracted from all parts of both male and female bodies during intercourse.  It was thought that the characteristics of the offspring are determined by the relative amounts and strength of fluids from each part of the body of each parent.

On the other hand, ‘preformationist’ theories held that the new mammalian offspring is already preformed in miniature, either within the egg of its mother or in the semen of its father.  Both of these types of theories incorporated ‘encasement’, which was the thesis that God created all future organisms in miniature, and that reproduction was just the growth and development of these miniatures.

Hippokratic theories were very good at explaining inheritance but very bad at explaining growth and development; whilst preformationist theories were the opposite – very good at explaining growth and development but very bad at explaining inheritance.  To give some examples, Hippokratic theories were unable to adequately explain phenomena such as the regeneration of freshwater polyps; while preformationist theories were unable to adequately explain how the mating of a mare with a donkey produces a mule.

Darwin came to his hypothesis of pangenesis, from a different direction – to fill a gap left in his theory of evolution.  Darwin’s breeding experiments on domestic animals (mainly pigeons) in the 1850s and 60s were part of his attempts to complete his evolution theory.  He was attempting in these experiments to show just how quickly varying characteristics can be amplified by domestic breeding, and therefore how natural selection can operate.

Darwin called his explanation of inheritance ‘the hypothesis of Pangenesis’, which he published in 1868.  However, he provides a more succinct description of this hypothesis in an earlier unpublished manuscript on pangenesis sent to Thomas Huxley in 1865:

“Furthermore, I am led to believe from analogies immediately to be given that protoplasm or formative matter which is throughout the whole organisation, is generated by each different tissue and cell or aggregate of similar cells; – that as each tissue or cell becomes developed, a superabundant atom or gemmule as may be called of the formative matter is thrown off; – that these almost infinitely numerous and infinitely minute gemmules unite together in due proportion to form the true germ; – that they have the power of self-increase or propagation; and that they here run through the same course of development, as that which the true germ, of which they are to constitute elements, has to run through, before they can be developed into their parent tissues or cells. This may be called the hypothesis of Pangenesis”.

pangenesis

The Laws of Inheritance & Pangenesis

Darwin further proposed that his hypothesis would not only account for inheritance, but also for development:

“The development of each being, including all the forms of metamorphosis and metagenesis, as well as the so-called growth of the higher animals, in which structure changes, though not in a striking manner, depends on the presence of gemmules thrown off at each period of life, and on their development, at a corresponding period, in union with the preceding cells”.

Through these mechanisms, Darwin proposed that inheritance and development were tied together – not only in the generation of offspring and early stages of embryonic life, but throughout the life of the organism.  By giving ‘gemmules’ the power to be modified throughout the life of an organism and then be transferred to the next generation, he argued that inheritance should be viewed as a form of growth.

By means of this single hypothesis, Darwin attempted to not only fill a gap in his theory of evolution, but whether he meant to or not, he created an apparent synthesis between the then competing paradigms relating to inheritance and development.

After reading Variation Under Domestication, Francis Galton (a cousin of Darwin’s) arranged for a series of experiments to be conducted on rabbits initially housed in the Zoological Gardens of London and later at his Kensington home.  His intention was to demonstrate the transmission of ‘gemmules’ to succeeding generations via blood injected from one rabbit to another, using coat colour as a marker.  Galton ultimately found that not a single instance of induced variation of coat colour occurred in a total of 88 offspring from blood transfused parents, and in 1871 published his results in Nature.

In later editions of Variation Under Domestication, Darwin admitted in a footnote that he would have expected to find ‘gemmules’ in the blood, although their presence was not absolutely necessary to his hypothesis.  Darwin’s response is unconvincing, as he provides no alternative explanation as to how the ‘gemmules’ are transmitted from the parents’ somatic cells to the germ cells.  He made no real attempt to modify his hypothesis in response to Galton’s falsification of it, indicating a possible abandonment of commitment to his hypothesis.

After the rediscovery of Mendel’s work in the 1890s, scientists tried to determine which molecules in the cell were responsible for inheritance.  In 1910, Thomas Hunt Morgan argued that genes are on chromosomes, based on observations of a sex-linked white eye mutation in fruit flies.  In 1913, his student Alfred Sturtevant used the phenomenon of genetic linkage to show that genes are arranged linearly on the chromosome.  It was soon discovered that chromosomes consisted of DNA and proteins, but DNA was not identified as the gene carrier until 1944. Watson and Crick’s breakthrough discovery of the chemical structure of DNA in 1953 finally revealed how genetic instructions are stored inside organisms and passed from generation to generation.

In view of the fact that it took another 85 years after Darwin’s book Variation Under Domestication before the molecular mechanisms of inheritance to be discovered, Darwin can hardly be blamed for getting it wrong way back in 1868.  This was before even chromosomes had been discovered, let alone DNA.

On the plus side, Darwin’s theory of evolution by natural selection, with its tree-like model of branching common descent, has become the unifying theory of the life sciences. The theory explains the diversity of living organisms and their adaptation to the environment. It makes sense of the geologic record, biogeography, parallels in embryonic development, biological homologies, vestigiality, cladistics, phylogenetics and other fields, with unrivalled explanatory power; it has also become essential to applied sciences such as medicine, agriculture, conservation and environmental sciences.

References

Darwin, Charles (1859) The Origin Of Species. 6th ed. 1873. London: John Murray.

Darwin, Charles (1875) The Variation of Animals and Plants Under Domestication, Vol II London: John Murray.

Mayr, Ernst (1982) The Growth of Biological Thought: Diversity, Evolution, and Inheritance Harvard University Press.

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DNA and GM foods

by Tim Harding B.Sc

(An edited version of this essay was published in The Skeptic magazine, September 2014, Vol 34 No 3, under the title ‘The Good Oil’.  The essay is based on a talk presented to the Mordi Skeptics, Tuesday 5 April 2011; and later to the Sydney Skepticamp, 30th April 2011.)

In May 2014, a farmer accused of ‘contaminating’ his neighbour’s land with genetically modified canola won a highly publicised civil case in the Western Australian Supreme Court (Marsh v. Baxter, 2014).  Although the case was about a claim of conflicting land use rather than food safety, it fired up the long-running community debate about genetically modified foods in Australia.  It also exposed a lot of misinformation and misunderstanding about DNA and genetic modification.

This essay discusses the nature and structure of DNA; together with the history of its discovery. It makes the point that artificial selection been occurring since the dawn of civilisation; and that the outcome of different methods of artificial selection is the same – modification of the genetic code by human intervention. Not only is there no evidence that genetically modified foods are unsafe to eat, but there is no mechanism by which they could be unsafe.

Brief history of DNA research

The rules of genetics were largely understood since Gregor Mendel’s ‘wrinkled pea’ experiments in the 1860s but the mechanisms of inheritance remained a mystery.   Charles Darwin knew in the 1850s there must have been such a mechanism (but his later speculations about it – called pangenesis – were wrong).[1]  The units of inheritance were called genes, but it was not understood where genes were located in the body or what they physically consisted of.

After the rediscovery of Mendel’s work in the 1890s, scientists tried to determine which molecules in the cell were responsible for inheritance.  In 1910, Thomas Hunt Morgan argued that genes are on chromosomes, based on observations of a sex-linked white eye mutation in fruit flies.  In 1913, his student Alfred Sturtevant used the phenomenon of genetic linkage to show that genes are arranged linearly on the chromosome.  It was soon discovered that chromosomes consisted of DNA and proteins, but DNA was not identified as the gene carrier until 1944.

Watson and Crick’s breakthrough discovery of the chemical structure of DNA in 1953 finally revealed how genetic instructions are stored inside organisms and passed from generation to generation.[2]  In the following years, scientists tried to understand how DNA controls the process of protein production. It was discovered that the cell uses DNA as a template to create matching messenger RNA (a single-strand molecule with nucleotides, very similar to DNA). The nucleotide sequence of a messenger RNA is used to create an amino acid sequence in protein; this translation between nucleotide and amino acid sequences is known as the genetic code.

DNA structure

The molecular basis for genes is deoxyribonucleic acid (DNA) a double-stranded molecule, coiled into the shape of a double-helix.  DNA is composed of twin backbones of sugars and phosphate groups joined by ester bonds.  These backbones hold together a chain of nucleotides, of which there are four types: adenine (A), cytosine (C), guanine (G), and thymine (T).  Genetic information in all living things exists in the sequence of these nucleotides, and genes exist as stretches of sequence along the DNA chain.[3]  Each nucleotide in DNA preferentially pairs with its partner nucleotide on the opposite strand: A pairs with T, and C pairs with G using weak hydrogen bonds.  Thus, in its two-stranded form, each strand effectively contains all necessary information, redundant with its anti-parallel partner strand.  This structure of DNA is the physical basis for inheritance: DNA replication duplicates the genetic information by enzymes splitting the strands (like a zipper) and using each strand as a template for synthesis of a new partner strand.

Chemical structure of DNA (Source: Wikimedia Commons)

Chemical structure of DNA (Source: Wikimedia Commons)

The sequence of these nucleotides A, C, G and T is a code, similar to the binary digital code used in computing.  When you consider that all the instructions for everything that computers can produce: text, calculations, music and images is stored as a binary sequence of ones and zeros, it is not hard to conceive how the instructions for making and operating living organisms can be stored as a four letter code.

Genes are arranged linearly along very long chains of DNA sequence, which comprise the chromosomes.  In bacteria, each cell usually contains a single circular chromosome, while eukaryotic organisms (including plants and animals) have their DNA arranged in multiple linear chromosomes.  These DNA strands are often extremely long; the largest human chromosome (No. 1), for example, is about 247 million base pairs in length. The full set of hereditary material in an organism (usually the combined DNA sequences of all 46 chromosomes in humans) is called the genome (approx. 3 billion base pairs in humans).

The genetic code is the set of rules by which information encoded in genetic material (DNA or mRNA sequences) is translated into proteins (amino acid sequences) by living cells.  The code defines a mapping between tri-nucleotide sequences, called codons, and amino acids. With some exceptions, a triplet codon in a nucleic acid sequence specifies a single amino acid.[4]

Translation of genetic code into proteins (Source: Wikimedia Commons)

Translation of genetic code into proteins (Source: Wikimedia Commons)

However, the human genome contains only ca. 23,000 protein-coding genes, far fewer than had been expected before its sequencing.  In fact, only about 1.5% of the genome codes for proteins, while the rest consists of non-coding RNA genes, regulatory sequences, introns, and noncoding DNA (once known as ‘junk DNA’). Genetic recombination during sexual reproduction involves the breaking and rejoining of two chromosomes (one from each parent) to produce two new rearranged chromosomes, thus providing genetic diversity and increasing the efficiency of natural selection.

Genetic modification

One of the biggest public misunderstandings is about the very term ‘genetic modification’.  Genes can be modified in 2 main ways:

Artificial selection can occur in 4 main ways:

  • traditional plant and animal breeding (long-term);
  • mutagenesis (random exposure to chemical or radiological mutagens);
  • RNA interference (switching genes on or off);
  • genetic engineering (short-term) – the targeted insertion or deletion of genes in the laboratory (which cannot easily be achieved by other methods).

The end result of the different methods of artificial selection is the same – modification of the genetic code by human intervention.  All DNA, whether modified naturally or artificially, is biochemically and nutritionally the same.  The only difference is in the genetic code, that is, the sequence of the bases G, C, T and A.  In other words, DNA is DNA – there are no such thing as ‘natural DNA’ and ‘artificial DNA’.

They are all ways of artificially modifying genes, yet for some illogical reason plant and animal breeding is not usually referred to in the media as genetic modification – possibly because it started a long time (c. 11,000 years ago) before genetics was understood.  However, to avoid any confusion, in this paper I will refer to genetic modification of foods by genetic engineering as genetically engineered foods (GE foods).

As a result of artificial selection, all farmed foods we eat today have been genetically modified by humans via plant and animal breeding.  This includes all meats except for wild game and kangaroo; and most farmed fish such as salmon.

Similarly all plants we eat (vegetables, fruits,  nuts, herbs and spices) have been genetically modified by humans.  Many varieties bear little resemblance to their original wild forms.  A wheat grain is a genetically modified grass seed.  Can anybody think of a plant food that has not been modified by humans?  (The only ones any of us at the meetup could think of were bush tucker, which is rarely found in Australian shops or supermarkets.  Seaweed was later suggested at the Sydney Skepticamp).

Whenever we eat and digest proteinaceous food, the DNA inside the food gets broken down into single nucleotides before absorption in the small intestine, destroying the genetic code anyway.  It is therefore logically impossible for any changes in the genetic code, whether artificial or natural, to make DNA unsafe to eat.

Not only is it logically impossible, but there is no empirical evidence that genetically modified foods are harmful.  The technology to produce genetically engineered (GE) plants is now over 30 years old, yet in all that time there has not been a single instance of anybody becoming ill, let alone dying, as a result of eating GE foods.

In a recent major review of the scientific literature on last 10 years of the world’s GE crop safety research, the reviewers conclude that ‘the scientific research conducted so far has not detected any significant hazard directly connected with the use of GE crops’.  The authors further believe that ‘genetic engineering and GE crops should be considered important options in the efforts towards sustainable agricultural production’ (Nicolia et al, 2013).

GE foods

GE foods can be produced by either cisgenesis (within the same species) or transgenesis (from different species).[5]  However, the point needs to be made that the human genome naturally contains genes resulting from billions of years of evolution – even genes from our fishy ancestors.  A substantial fraction of human genes seem to be shared among most known vertebrates.  For example, the published chimpanzee genome differs from that of the human genome by 1.23% in direct sequence comparisons.  We also share many genes with plants.

“The real question here is not whether there is a GMO tomato with a fish gene, but who cares? It’s not as if eating fish genes is inherently risky—people eat actual fish. Furthermore, by some estimates people share about 70 percent of their genes with fish. You have fish genes, and every plant you have ever eaten has fish genes; get over it.”[6]

GE foods were first put on the market in the early 1990s.  Typically, genetically modified foods are transgenic plant products: soybean, corn, canola, and cotton seed oil.  

GE genes may be present in whole foods, such as wheat, soybeans, maize and tomatoes.  The first commercially grown genetically modified whole food crop was a tomato (called FlavrSavr), which was modified to ripen without softening, in 1994.  These GE whole foods are not presently available in Australia.  GE food ingredients are, however, present in some Australian foods.  For example, soy flour in bread may have come from imported GE soybeans.[7]

In addition, various genetically engineered micro-organisms are routinely used as sources of enzymes for the manufacture of a variety of processed foods. These include alpha-amylase from bacteria, which converts starch to simple sugars, chymosin from bacteria or fungi that clots milk protein for cheese making, and pectinesterase from fungi which improves fruit juice clarity.

sugar

Genetic engineering can also be used to increase the amount of particular nutrients (like vitamins) in food crops. Research into this technique, sometimes called ‘nutritional enhancement’, is now at an advanced stage. For example, GE golden rice is an example of a white rice crop that has had the vitamin A gene from a daffodil plant inserted. This changes the colour and the vitamin level for countries where vitamin A deficiency is prevalent. Researchers are especially looking at major health problems like iron deficiency. The removal of the proteins that cause allergies from nuts (such as peanuts and Brazil nuts) is also being researched.[8]

Animal products have also been developed, although as of July 2010 none are currently on the market.  However, human insulin has been produced using GE E.coli bacteria since 1978.  In 2006 a pig was controversially engineered to produce omega-3 fatty acids through the expression of a roundworm gene.  Researchers have also developed a genetically-modified breed of pigs that are able to absorb plant phosphorus more efficiently, and as a consequence the phosphorus content of their manure is reduced by as much as 60%.

Once again, there is no evidence of any person being harmed by eating genetically engineered foods.  The reasons why genetically engineered whole foods are not yet available in Australia are political or emotional rather than scientific.

Benefits of GE foods

There is a need to produce inexpensive, safe and nutritious foods to help feed the world’s growing population. Genetic engineering may provide:

  • Sturdy plants able to withstand weather extremes (such drought);
  • Better quality food crops;
  • Higher nutritional yields in crops;
  • Inexpensive and nutritious food, like carrots with more antioxidants;
  • Foods with a greater shelf life, like tomatoes that taste better and last longer;
  • Food with medicinal (nutraceutical) benefits, such as edible vaccines – for example, bananas with bacterial or rotavirus antigens;
  • Crops resistant to disease and insects and produce that requires less chemical application, such as pesticide and herbicide resistant plants: for example, GE canola.[8]

Objections to GE foods

So why is there such significant opposition to GE foods from some vocal lobby groups? Critics have objected to GE foods on several grounds, including:

  • the appeal to nature fallacy (natural products are good and artificial products are bad);
  • alleged but unproven safety issues, (there is no evidence of any adverse health effects, including allergies, in the 20 years since GE foods became available);
  • marketing concerns about ‘contamination’ of so-called organic food crops by GMOs (such as in the Marsh -v-Baxter case);
  • ecological concerns about the spread of GMOs in the wild, and
  • economic or ideological concerns raised by the fact that these organisms are subject to intellectual property rights usually held by big businesses.

The only one of these objections that may have any scientific legitimacy is the ecological concern about the spread of GMOs in the wild.  However, the use of GE technology is highly regulated by Australian governments and any such ecological concerns are fully taken into account.

Current food regulations in Australia state that a GE food will only be approved for sale if it is safe and is as nutritious as its conventional counterparts.  Food regulatory authorities require that GE foods receive individual pre-market safety assessments prior to use in foods for human consumption.  The principle of ‘substantial equivalence’ is also used.  This means that an existing food is compared with its genetically modified counterpart to find any differences between the existing food and the new product.  An important to note is that Australia has the most rigorous food safety testing regime in the world, and that GE foods are tested even more rigorously than non-GE foods. Because of this higher level of testing, GE foods are likely to be safer than non-GE foods.

Foods certified as organic or biodynamic should not contain any GE ingredients, according to voluntary organic food industry guidelines.

Here is a list of 114 peer-reviewed articles and meta reviews, mostly published in moderate to high impact factor journals that support the safety of GMO crops over a wide range of hypotheses.  The consensus position of the American Association for the Advancement of Sciences on GM foods is:

“Indeed, the science is quite clear: crop improvement by the modern molecular techniques of biotechnology is safe… The World Health Organization, the American Medical Association, the U.S. National Academy of Sciences, the British Royal Society, and every other respected organization that has examined the evidence has come to the same conclusion: consuming foods containing ingredients derived from GM crops is no riskier than consuming the same foods containing ingredients from crop plants modified by conventional plant improvement techniques.”

References

American Association for the Advancement Of Science (2012). Statement by the AAAS Board of Directors On Labeling of Genetically Modified Foods. 20 October 2012.

Better Health Channel (2011) Fact Sheet – Genetically modified foods www.betterhealth.vic.gov.au Melbourne: State of Victoria.

Darwin, Charles (1868),The Variation of Animals and Plants under Domestication (1st ed.), London: John Murray.

Lynas, Mark (29 April 2013) Time to call out the anti-GMO conspiracy theory.  Mark Lynas speech hosted by the International Programs – College of Agriculture and Life Sciences (50th Anniversary Celebration) , and the Atkinson Center for a Sustainable Future, Cornell University.

Marsh -v-Baxter [2014] WASC 187 (28 May 2014).

Nocolia, A., Mazo, A., Veronesi, F., and Rosellini (2013) ‘An overview of the last 10 years of the genetically engineered crop safety research’. Critical Reviews in Biotechnology. Informa Healthcare USA Inc. ISSN: 0738-8552 (print) 1549-7801 (electronic).

Skeptical Raptor’s Blog. What does science say about GMO’s–they’re safe. Updated 19 November 2014.

Novella, Stephen (2014) ‘No Health Risks from GMOs’. The Science of Medicine .Volume 38.4, July/August 2014.

Watson J.D. and Crick F.H.C. (1953) A Structure for Deoxyribose Nucleic Acid. Nature 171 (4356): 737–738.

Other information is from Wikipedia and the author’s knowledge as a former biochemist.  (According to convention, anonymous Wikipedia pages, whilst thought to be mostly factually correct, are not citable as references).


[1] Darwin, 1868.

[2] Watson and Crick, 1953.

[3] Viruses are the only exception to this rule—sometimes viruses use the very similar molecule RNA instead of DNA as their genetic material.

[4] Not all genetic information is stored using the genetic code. All organisms’ DNA contains regulatory sequences, intergenic segments, and chromosomal structural areas that can contribute greatly to phenotype by controlling how the genes are expressed.  Those elements operate under sets of rules that are distinct from the codon-to-amino acid paradigm underlying the genetic code.

[5] For example, the gene from a fish that lives in very cold seas has been inserted into a strawberry, allowing the fruit to be frost-tolerant.  However, this has not as yet been done for currently available commercial food crops.

[6] Novella, 2014.

[7] Better Health Channel, 2011.

[8] Better Health Channel, 2011.

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