Select Committee on European Communities Minutes of Evidence

Written material from Professor Mark Williamson, Professor Emeritus of Biology, University of York



  There is some dispute about whether the study of invasions is relevant to the assessment of risks from the release of genetically engineered organisms. So, first, what are these organisms and why should there be risks?

  Molecular genetics now allows a gene to be taken from one organism and inserted into some totally unrelated one. Bacterial genes can be put into plants, arthropod genes into viruses. There are, of course, limits on what can be done but, as the subject is moving fast, I will not dwell on them here. This transfer of genes is commonly called genetic engineering. The current fashion is to refer to genetically modified organisms, or GMOs, rather than genetically engineered ones, and that is followed in official documents. For scientists, there is no reason to prefer an ambiguous and obscure term to one that is reasonably precise (Williamson, 1992). Genetic modification is a term that can be applied to all genetic programmes, and has no obvious association with restriction enzymes and the other tools of molecular geneticists. Genetic engineering is less ambiguous, and gives the flavour of experimental manipulation, so I will use it here. It is also the term used in US Congress OTA (1993).

  Genetic engineering can be used to make organisms with new properties that may be commercially useful. In crop plants, herbicide- and pest-resistant varieties are being developed in many species. It is possible to change the nature of the crop product, changing the composition of the oil in oil seeds, manipulating enzymes so that tomatoes do not go squashy, and many other features. Pharmaceuticals could be made in plants or produced in milk. Fish can be made to grow faster (US Congress OTA, 1993; Krattiger and Rosemarin, 1994).

  In principle, any commercially desirable trait could be added or enhanced. It is not surprising that much research has been funded, and that many commercial releases are near. On Krattiger's (1994) count there have been 2,053 field trials of transgenic plants world-wide up to mid-1994, and that, even allowing for differences in the definition of a trial, is fairly certainly too low (Anon, 1994b). Although almost all OECD countries have some form of regulation, others outside the OECD such as China and Israel apparently do not. Regulation, such as the European Union's directive 90/220/EEC, is likely to keep only a few, rather obviously undesirable, products from the market. It is reasonable to assume that there will soon be many different genetically engineered organisms marketed in large numbers world-wide.

  Will there be ecological and environmental change from genetically engineered organisms? Russo and Cove (1995) give a good overview of all the benefits and hazards from these techniques. Invasions show that damage can happen when an organism finds itself in a new environment. For a novel genetically engineered organism all environments are new. A familiar case where a change to a new environment, accompanied by a small genetic change, has had quite unforeseen terrible effects is AIDS. Maybe some day a genetically engineered organism will produce a major, but quite different, disaster.

  Human AIDS is caused by two viruses, HIV1 and HIV2. These are closely related to a group of viruses found in other primates, the Simian Immunodeficiency Viruses or SIVs (Morrison and Desrosiers, 1994). These are all single-stranded, encapsulated RNA viruses, retroviruses. Being RNA viruses, they are far less stable genetically than DNA organisms. Various strains in one virus have 80 to 100 per cent identity, closely related retroviruses attacking other species have about 80 to 90 per cent identity, more widely related ones 55 to 60 per cent. It would seem that both HIV2 and SIVmac (which infects captive macaques, Macaca) are derived from SIVsmm (which infects the sooty mangaby, Cercocebus torquatus). Similarly, HIV1 is closely related to SIVcpz which is found in chimpanzee Pan troglodytes. SIVs in wild monkeys and apes are, as far as is known, non-pathogenic. Rhesus monkeys Macaca mulatta with SIVmac develop an AIDS-like disease. Pigtail macaque M. nemestrina with the same virus are killed in a week or so. Small genetic changes and a new environment can produce very drastic effects.

  As I said at the end of section 5.3.1, major invasions may come out of the blue at any time. Will genetically engineered organisms add to these problems?

  Some proposals, such as the engineering of non-specific biological control viruses, are evidently bad practice (Williamson, 1991), but the unnecessary risk comes from the nature of the virus, not the genetic engineering. It is often asserted that for most commercial genetic engineering, the invasion model is not appropriate. For instance, with crop plants, the argument is that the plant is familiar, the new variety will have to undergo extensive performance trials, and the genetic novelty is more precise and better understood than the genetic novelty produced by traditional breeding programmes. Hence the release of genetically engineered plants is different from other invasions. It is also sometimes stated that many changes are needed to change an organism into a weed or a pathogen (National Academy of Sciences, 1987).

  The unsatisfactory points in that argument are covered in earlier sections of this book. Although the crop plant is familiar, and the genes inserted are well known, the combination is novel. There are no universal characters that distinguish weeds and pathogens from their harmless relatives (section 3.3.2), and the genetic differences between invasive species and those that fail to invade may often be small (section 6.2). In fact, many plants have become weeds merely by being taken to new regions. It is not surprising that ecologists think that aspects of the invasion model are relevant to the risk assessment of genetically engineered organisms (Tiedje et al., 1989; Altmann, 1993; Shorrocks 1993; US Congress OTA, 1993; Seidler and Levin, 1994). It is an appropriate model.

  Even in those countries where there is effective regulation of small-scale trials, the study of invasions suggests that the probability of detecting undesirable products at an early stage is not large. Many pest invaders have not been recognised as such for many years, often decades, Impatiens glandulifera (section 1.3.3) and the muntjac deer (section 5.1) for example. On the other hand others, such as zebra mussel (section 5.4) were recognised as problems almost immediately, but spread so fast that it was difficult to limit the damage. As those genetically engineered organisms that become problems will usually be commercial products, they will mostly be widespread quickly, and difficult to control whether the problem arises soon or not.

  Some problems may well be delayed. Texas cytoplasm is a possible example of how this could happen; it is a genetic modification of corn, Zea mays. In corn, male sterility is a most useful agronomic trait, because it allows controlled breeding without the work of removing the male inflorescences, the tassels. Texas Cytoplasm varieties are male sterile because of a change in a mitochondrial gene (Levings, 1990). Remarkably, the same molecular mechanism that made the plants male-sterile also made the plants susceptible to a fungal pathogen, Bipolaris maydis race T. About two decades after the gene, T-urf13, came into commercial use, the fungal disease devastated the corn containing that gene, which was by that time 85 per cent of the US corn hectarage, and made the innovation useless. The molecular details were known, the pathogen was known, but the interaction was not predicted and the consequences did not appear until the new genotype was in full commercial use. It seems optimistic to suppose that similar failures will not happen in future, however the regulatory system is designed. Without regulation they might even become common.

  Texas cytoplasm was an agronomic problem. Will there be ecological and conservation problems? There are two classes of possibility. One is the spread of the genetically engineered organism itself, the other is the spread of the engineered gene in wild relatives of that organism (Raybould and Gray, 1993). As with all invasions, and bearing the tens rule in mind (section 2.3), it is reasonable to say that neither will happen frequently. Pests arise in around 1 per cent of organisms introduced at random. If regulators can control excessive commercial enthusiasm, the frequency could be much less (Williamson, 1988); that is taking an optimistic view of the effectiveness of regulators and regulations. But whatever the proportion, the number of proposed products is so large, that some ecological damage seems likely, though it may not be apparent for some decades.

  Perhaps the most remarkable general feature of invasions is how unpredictable they are. One possible gain from the release of genetically engineered organisms may be a better understanding of why most genetic variation seems to have no relation to invasion success, but nevertheless some genes are important.

previous page contents next page

House of Lords home page Parliament home page House of Commons home page search page enquiries

© Parliamentary copyright 1999