Tag Archives: evolution

Theories of Generation

by Tim Harding

Does Darwin successfully combine the two explanatory paradigms of inheritance, and growth and development?  If he does, is this a problem for Kuhn’s view of scientific change?

In this essay, I intend to show how Darwin’s hypothesis of pangenesis created a synthesis between the then competing paradigms relating to inheritance and development.  I think that this synthesis does present a problem for Kuhn’s view of scientific change, and that Popper’s account may actually be more relevant than Kuhn’s to certain aspects of this particular case study.

Before discussing Darwin’s theories, it is necessary to briefly describe the two paradigms that attempted to explain inheritance (how characteristics are transferred to offspring from parents), and growth and development (how the growth of offspring is organised).  These two paradigms were characterised by competing Hippocratic theories and preformationist theories (Verdnik, 1998:126, 157).

Before the advent of genetics, Hippocratic 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 (Verdnik, 1998:126).

On the other hand, preformationist theories held that the new mammalian offspring is already preformed in miniature, either within the egg of its mother (ovist preformationism) or in the semen of its father (animalculist preformationism).  Both of these types of theories incorporated emboîtment (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 (Verdnik, 1998:128).

Hippocratic 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 (Verdnik, 1998:126).  To give some examples, Hippocratic theories were unable to adequately explain phenomena such as the regeneration of freshwater polyps as observed by Trembley (Trembley 1744: 148); while preformationist theories were unable to adequately explain how the mating of a mare with a donkey produces a mule (Maupertuis 1745: 172).

Darwin came to his hypothesis of pangenesis, from a different direction – to fill a gap left in his theory of evolution, as published in his 1859 book The Origin of Species (Darwin, 1859).  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.  Darwin’s breeding experiments on domestic animals (mainly pigeons) in the 1850s and 60s[1] were part of his attempts to complete his evolution theory (Bartley, 1992: 308).  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 (Verdnik, 1998:156).


The Laws Of Inheritance & Pangenesis

Darwin called his explanation of inheritance ‘the hypothesis of Pangenesis’, which he published in Part II of Chapter XXVII of Variation Under Domestication (Darwin, 1875: 374-404).  However, he provides a more succinct description of this hypothesis in an earlier unpublished manuscript on pangenesis sent to 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’ (Olby 1963: 259).

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 ‘ (Darwin, 1875: 403-404).

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 (Bartley, 1992: 310).  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 (Bartley, 1992: 331).

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

The preceding discussion raises some significant philosophical issues.  How does it compare with Kuhn’s view of scientific change; and in particular, is Darwin’s paradigm synthesis a problem for the Kuhnian account?

According to Kuhn, ‘normal science’ operates within scientific paradigms[2] that not only determine which scientific theories are acceptable, but define scientific communities and even the areas of research undertaken (Kuhn, 1962: 10-11).

Kuhn says that in so far as he is engaged in normal science, the researcher is a solver of puzzles, not a tester of paradigms.

Paradigm-testing occurs only after persistent failure to solve a noteworthy puzzle has given rise to crisis.  And even then it occurs only after the sense of crisis has evoked an alternative candidate for a paradigm.  In the sciences, the testing situation never consists, as puzzle-solving does, simply in the comparison of a single paradigm with nature.  Instead, testing occurs as part of the competition between two rival paradigms for the allegiance of the scientific community (Kuhn, 1962: 144-145).

Kuhn notes that the schools guided by different paradigms are ‘always slightly at cross-purposes’ and that they ‘fail to make complete contact with each other’s viewpoints’, a phenomenon which describes as ‘incommensurability’ (Kuhn, 1962: 112, 148-150).  The failure of the adherents of Hippocratic and preformationist theories to focus on the strengths and weaknesses of both paradigms, and to engage in the testing of both paradigms, tends to support Kuhn’s notion of incommensurability.  No crisis occurred within each paradigm, because their adherents failed to focus on how well each paradigm explained both inheritance and development.

The formulation of Darwin’s hypothesis does not accord with the Kuhnian account.  He did not conduct his breeding experiments on domestic animals to test either the Hippocratic or the preformationist paradigms, but to fill a gap in his quite separate theory of evolution.  Similarly, his synthesis between the then competing paradigms relating to inheritance and development, was not done to resolve any crisis in these paradigms, but for a separate purpose.  A further problem for the Kuhnian account is that the scientific method Darwin used to formulate his hypothesis was essentially inductive, although this may also be a problem for the Popperian account.

Another aspect of the Kuhnian account is that the failure of experimental results to conform to the prevailing paradigm is seen as an ‘anomaly’, rather than as an instance of Popperian falsification.[3]  If scientists are confronted by anomalies, they will often devise ad hoc modifications in order to eliminate any apparent conflict.  Anomalies do not cause the abandonment of paradigm or theory unless and until the level of anomalies builds to a crisis where the prevailing paradigm or theory is replaced by a new one (Kuhn, 1962: 77-78).

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 (Brown, 2002: 290-291).  Although intended to verify Darwin’s hypothesis, it seems that Galton’s experiments provided a Popperian falsification instance.  Whether the purpose was verification or falsification, Galton’s experiments do not accord with Kuhn’s account of paradigm-testing discussed above.

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 (Brown, 2002: 292).  I find Darwin’s response 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.

I therefore conclude that whilst the Hippocratic and preformationist paradigms accord with Kuhn’s notion of incommensurability, Darwin’s synthesis of these two paradigms does not accord with the Kuhnian account of science.  Furthermore, Darwin’s failure to make an ad hoc modification to his hypothesis after the discovery by Galton of an anomaly, as would be expected under the Kuhnian account, supports a Popperian rather than a Kuhnian account of the scientific process in this case.


Bartley, M.M. (1992) Darwin and Domestication: Studies on Inheritance. Journal of the History of Biology, Vol 25, No. 2 pp.307-333.

Browne, J. (2002) Charles Darwin – The Power of Place, Volume II of a Biography. London: Pimlico.

Darwin, C. (1859) The Origin Of Species By Means Of Natural Selection, Or The Preservation Of Favoured Races In The Struggle For Life. 6th ed. 1873. London: John Murray.

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

Kuhn, T.S. (1962) The Structure of Scientific Revolutions 3rd ed. Chicago: University of Chicago Press.

Maupertuis, P. (1745) The Earthly Venus in Verdnik, D. (ed.) (1998) Thinking about Science. Study Guide and Readings. Churchill: Monash Distance Education Centre.

Olby, R.C. (1963) Charles Darwin’s Manuscript of Pangenesis, British Journal for Philosophy of Science 1: 251-263.

Popper, K. (1959) The Logic of Scientific Discovery. rev. ed. 1968, in Verdnik, D. (ed.) (1998) Thinking about Science. Study Guide and Readings. Churchill: Monash Distance Education Centre.

Trembley, A. (1744) Memoires pour server a l’histoire d’un genre de polypes d’eau douce in Verdnik, D. (ed.) (1998) Thinking about Science. Study Guide and Readings. Churchill: Monash Distance Education Centre.

Verdnik, D. (ed.) (1998) Thinking about Science. Study Guide and Readings. Churchill: Monash Distance Education Centre.


[1] Darwin reported the results of these experiments in both The Origin Of Species and The Variation of Animals and Plants Under Domestication.

[2] Kuhn does not provide a concise definition of a scientific paradigm, but the Merriam-Webster Online dictionary defines it as ‘a philosophical and theoretical framework of a scientific school or discipline within which theories, laws, and generalizations and the experiments performed in support of them are formulated; broadly: a philosophical or theoretical framework of any kind.’

[3] Popper proposes falsifiability as the criterion of demarcation between scientific and non-scientific statements.  In other words, a theory is scientific if it is falsifiable (Verdnik, 1998:76).

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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.


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.”


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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