Science in Society Archive

Letter To The Scottish Parliament Petitions Committee

Institute of Science in Society
Director: Dr. Mae-Wan Ho

Date: 28 February 2002
To: Scottish Parliament Petitions Committee
From: Dr. Mae-Wan Ho

I am writing to support the Munlochy Vigil petition, to call for an immediate end to GM OSR trials in Scotland and for a full Parliamentary debate, with a free vote on the issue of GM crops in Scotland. I wish to state my reasons for opposing the introduction of GM crops to the UK in the farm scale evaluations, in particular to Aventis’ GM oilseed rape, which is being field-tested in Scotland.

GM crops are of no benefit to farmers or consumers and harmful to the environment

Since the commercial growing of GM crops in 1994, there have been many university-based studies documenting that they have lower yields, perform poorly in the field, use more pesticides and result in reduced profits for farmers. The details are contained in a new report [1] from the Institute of Science in Society (ISIS), of which I am Director.

GM crops place control of food production in the hands of corporations, taking away our right to self-determination and the livelihood of farmers

This is done through patenting of GM crops and genes and draconian measures to prevent farmers from saving seeds, through GM crops linked to herbicides sold by corporations, and worst of all, through crops engineered to make the plants or seeds sterile. Aventis’ GM oilseed rape is engineered to be male sterile, for the stated reason of producing ‘high-yielding’ hybrid; but the real reason is to protect corporate patents.

GM crops contain new genes and gene products of unproven safety at best, or known to be harmful

ISIS has covered the hazards of GM crops extensively, and is including several reprint collections for your perusal [2-4]. Genes incorporated into GM crops are typically from bacteria and viruses that cause diseases, and include antibiotic resistance marker genes that could make infectious diseases untreatable. These genes and gene products have never been part of the food chain of either human beings or many of the animals that feed on the plants.

The endotoxins isolated from the soil bacterium Bacillus thuringiensis (bt) are known to be harmful to beneficial insects such as the lacewings and endangered species such as the monarch butterfly, as well as to rodents.

The barnase gene used for making male-sterile lines, such as Aventis’ GM oilseed rape, is a universal cell poison that requires a very specific antidote, it has been shown to be toxic to the rat kidney and to human cell lines.

Broad spectrum herbicides used with GM crops destroy all species of plants, and are also toxic to insects, mammals and human beings

Glufosinate herbicide, used with many GM crops including Aventis GM oilseed rape, is known cause birth defects [5-7] and to damage nerve cells [8,9]. It has also been found to harm predatory insects and mites [10] and caterpillars of the skipper butterfly Calpodes ethlius [11]. This will have knock-on effects on the survival of birds. The field trials in Scotland are close to some of the most precious wild-life preserves. The run-off from Roskill Farm, for example, goes directly into the Munlochy Bay, thereby contaminating the drinking water for both wildlife and human beings.

Herbicide tolerant GM crops become superweeds through gene stacking

A 1998 study in Canada revealed that herbicide-tolerant oilseed rape rapidly evolved into superweeds through accumulating multiple herbicide-tolerant traits - a phenomenon referred to as ‘gene-stacking’ [12]. A new report by English Nature [13] draws attention to the same findings in 11 further fields in Alberta, Canada, and also in field trials in the United States. It concludes that such gene-stacking for multiple herbicide tolerances are inevitable, and would necessitate using additional herbicides to control these volunteers.

Stability of GM crops is unproven

The safety of GM crops was strongly contested by scientists and others during the Chardon LL hearing held in the UK the year before last. Perhaps most relevant to the issue of safety is the genetic stability and uniformity of GM crops. The public hearing on T25 was suspended over a year ago when it was found not to have passed the required EC test for Distinctiveness, Uniformity and Stability (the DUS test), as I pointed out when giving evidence to the hearing [14].

The new EC Directive on deliberate release (Directive 2001/18) requires strict molecular evidence of genetic stability, which is also necessary for establishing the identity of the transgenic line and to ensure traceability. The best-kept secret of GM crops is that they are not stable.

The severe stunting of the GM oilseed rape in Roskill Farm subsequent to the application of the glufosinate herbicide ( is an example of such instability. The glufosinate-tolerant GM crop has apparently lost its ability to tolerate the herbicide, and we urgently need to know why, for safety reasons.

There is a large literature on gene silencing, in which the transgenes remain in the genome, but are not expressed. More serious, from the safety point of view, is structural instability, the tendency for the transgenic DNA to come loose, to rearrange or become lost in part or in whole in successive generations (see [4,15]). This could change the transgenic line in unpredictable ways in terms of health and environmental risks. And it will increase the chance of transgenic DNA being taken up by unrelated species to make new combinations with their genetic material. That is referred to as horizontal gene transfer and recombination. Transgenic DNA can spread to every species that interacts with the transgenic plant, in the soil, in the air, in the mouth and gut and the respiratory tracts of animals including human beings.

New viruses and bacteria that cause diseases could be generated, and antibiotic resistance marker genes could spread to the pathogens. Transgenic DNA may also get into human cells and insert into the human genome; and a large body of evidence from so-called gene therapy experiments have amply demonstrated this does take place [16]. The constructs used in gene therapy are very similar to those used in transgenic plants, and one main ‘side-effect’ of transgenic DNA inserting into human genome during gene therapy is cancer.

Despite that, our regulators have not required biotech companies to provide molecular evidence of stability. ACRE’s latest guidelines for industry put out for public consultation asks industry to provide molecular evidence of genetic stability over one generation only [17], which is derisory. We need data for at least five successive generations [18]. No such data have come forward from the companies. On the contrary, companies have been allowed to hide under ‘commercial confidentiality’. And the available information provided is vague, contradictory and sometimes wrong, as in the case of Aventis’ GM oilseed rape.

Trangenic DNA is inherently unstable and more prone to horizontal gene transfer and recombination

Transgenic DNA is different from natural DNA, and is more likely to take part in horizontal gene transfer and recombination for the following reasons.

  • All artificial constructs tend to be unstable, so much so that this is a topic in a standard text-book on genetic engineering [19]. Transgenic DNA is more likely to break and join up again, ie, to recombine.
  • Transgenic DNA typically contains DNA from widely different sources, mainly bacteria and viruses and other genetic parasites that cause diseases and spread antibiotic resistance, and hence, has the potential to recombine homologously with all those agents, ie, due to similarities in DNA base-sequence. Homology enhances horizontal gene transfer 10 million to 100 million-fold [20].
  • Transgenic DNA is designed to cross species barriers and to invade genomes. They are flanked by recombination sequences, such as the left and right borders of T-DNA or the terminal repeats of viral vectors, which enable them to jump into genomes. By the same token, they could jump out again. Enzymes catalysing jumping in also catalyse jumping out.
  • Certain ‘receptive hotspots’ have now been identified in both the plant [21] and the human genome [22]. These may also be ‘recombination hotspots’, prone to breaking and rejoining. That would mean inserted transgenes are more likely to be lost, to recombine, or to invade other genomes.
  • There are mechanisms in the cell that actively seek out, inactivate or eliminate foreign DNA from the genome [23].
  • Cell and embryo culture methods are well-known to induce unpredictable. uncontrollable (somaclonal) variations that persist in the plants generated. There is now evidence that the transformation process for making transgenic plants induces further genetic instability [24-26] leading to chromosomal rearrangements, genome scrambling, in other words.
  • Monsanto’s Roundup Ready soya, commercially grown for years, was the only crop to be independently checked by molecular methods last year. Not only is the gene order of the insert found to be scrambled, the plant genome at the site of insertion is also scrambled, and there is a 534 bp fragment of unknown origin in there as well [27]. All very different from the original data provided by Monsanto.

In addition to the usual instability, certain constructs and sequences in the transgenic DNA can make it even more unstable, and hence more prone to horizontal gene transfer and recombination. These are as follows:

  • Recombination hotspots such as that associated with the ubiquitous cauliflower mosaic virus (CaMV) 35S promoter, could enhance horizontal gene transfer and recombination. We highlighted that in 1999 [28-30], and demanded all transgenic crops with the promoter should be immediately withdrawn for safety reasons. Two years later, the researchers who discovered the promoter’s recombination hotspot also recommended that it should no longer be used [31], not because of safety, but because its instability compromises agronomic performance.
  • Recently, landraces of corn growing in remote regions of Mexico were found contaminated with transgenic corn DNA by probing with the CaMV 35S promoter [32]. Molecular analysis showed that the sequences next to the promoter are very diverse, as consistent with horizontal gene transfer and recombination [33].
  • CaMV 35S promoter is active in species across the entire living world, including frog eggs and human cells [30] as we uncovered in the literature more than ten years old that had apparently escaped the notice of plant geneticists who attacked us. CaMV 35S promoter, if transferred to human or animal cells, could activate cancer-associated genes as well as dormant viruses that are in all genomes. Another side effect of gene-therapy is the generation of active viruses in cell lines used to package the gene-therapy vectors [16]. Our critics are still dismissing the risks of CaMV 35S promoter, but are avoiding doing any experiments. It is a case of don’t look, don’t see [18].

Aventis’ MS8/RF3 oilseed rape is the worst possible GM crop

MS8/RF3, which is being field tested in Scotland, is a genetically modified oilseed rape system for producing hybrid seeds. As stated earlier, it engineers the crop to be male sterile in order to protect corporate patents. Its gene products are hazardous.

It is very difficult to get a clear picture of the genetic modification because crucial molecular information is withheld from the public under ‘commercial confidentiality’, while the available information is vague, contradictory and even wrong.

As far as can be gathered, the system uses a gene for male sterility in the MS8 line, and a gene that restores male fertility in the RF3 line. Male sterility is achieved by a gene coding for barnase, which, as already mentioned, is a cell poison. It breaks down RNA, an intermediate in the expression of all genes. Fertility is restored by a gene coding for barstar, a specific inhibitor of barnase. Both barnase and barstar genes are derived from the soil bacterium, Bacillus amyloliquefaciens, and are placed under the control of a promoter (pTA29, from tobacco plant) that is expressed, in principle, only in the layer of cells surrounding the pollen sac during anther development. The expression of barnase kills the cells and blocks anther development in the MS8 line. When these plants without anthers are crossed with the line expressing the barstar gene (RF3), barnase is inactivated, and anther development proceeds, so the hybrid is fertile.

MS8, on account of being male-sterile, must always be fertilised by other lines. So, how can such a ‘line’ be maintained? The answer, according to some documents submitted, is that the barnase and barstar genes are both linked to a selective marker, phosphinothricin acetyltransferase gene (pat), originating from the soil bacterium Streptomyces hygroscopicus. It confers tolerance to glufosinate herbicide, which, as described above, not only kills all plants, but harms many animals including human beings.

However, in a letter [34] written in response to my enquiry, the Scottish Executive stated that the RF3 line was not tolerant to glufosinate, ie, the barstar gene was not linked to the pat gene.

In the documents submitted to the Scottish Executive, the pat gene is shown to be under the control of the cauliflower mosaic virus (CaMV) 35 S promoter (albeit in another line, though the implication is that the same construct is used for MS8/RF3). In applications to DEFRA for the same, ie MS8/RF3, the gene is stated to be under the control of another promoter.

In the documents submitted to the Scottish Executive, one criterion of genetic stability was stated to be segregation of two independent genes according to the ratio of 3:1, which is a howler, as two independent genes segregating, if both heterozygotes were dominant, would be 15:1. This highlights the frequent abuse of Mendelian ratios. Failure to find significant deviations from Mendelian ratios does not imply Mendelian inheritance, much less is it a criterion of genetic stability, particularly as the status of the parental line is not independently ascertained. Aventis has admitted Mendelian ratios do not indicate genetic stability during the recent ACRE public hearing on T25 GM maize [35].

By applying the glufosinate herbicide, plants not carrying the male sterility gene will be eliminated from the MS8 line. MS8 is therefore a permanent hybrid, probably maintained by always crossing with RF3, with non-hybrid plants eliminated by glufosinate.

In that case, MS8/RF3 hybrid will spread the male sterility gene through its pollen. As the barstar and barnase genes are not linked together, some of the pollen will be spreading the male sterility gene by itself. This could have large effects on non GM oilseed rape varieties as well as on wild relatives. Another casualty will be bees and human beings consuming honey, if the barnase gene became expressed as a result of horizontal gene transfer and recombination.

Of course, if MS8/RF3 is genetically unstable, as suggested by its failure to tolerate glufosinate in the Munlochy field trial, then all of its transgenic DNA could be taking part in horizontal gene transfer and recombination. Horizontal gene transfer is not just a theoretical possibility.

Transgenic DNA from GM plants has been found to transfer to soil bacteria [36]. The possibility of transfer to bacteria in the mouth and gut of animals was suggested in laboratory investigations funded by the UK government [3]. But ACRE has ignored the evidence by a selective interpretation of the scientific evidence that seems to me contrary to both the precautionary principle and good science [37].


GM crops should be firmly rejected as being both unethical and unsafe for health and the environment. On the contrary, Scotland should be supporting and promoting its thriving organic agriculture. There is now plenty of evidence that sustainable, organic agriculture is working all over the world [1]. GM crops are definitely not needed to feed the world. New research reveals that in many of the poorest African countries on the borders of the Sahara desert, introduction of integrated farming, mixed cropping and traditional water conservation methods are pushing back the desert [38] and increasing per capita food production several fold, keeping well ahead of population growth.

Article first published 28/02/02


  1. Lim LC and Matthews J. GM crops failed on every count, ISIS Report. In Ho MW, Cummins J, Ryan A et al, Hazards of GM Crops ISIS Reprints, ISIS Publications, London, March 2002.
  2. Ho MW, Cummins J, Ryan A et al, Hazards of GM Crops, ISIS Reprints, ISIS, London, March 2002.
  3. Ho MW, with Ryan A. Horizontal Gene Transfer, ISIS Reprints, ISIS, London, 2002.
  4. Ho MW, Cummins J, Ryan A. Transgenic Instability, ISIS Reprints, ISIS, London, March 2002.
  5. Watanabe, T. (1996). Developmental effects of glufosinate ammonium on mouse embryos in culture. Teratogenesis, Carcinogenesis and Mutagenesis 19, 287-99.
  6. Fujii, T. (1997). Transgenerational effects of maternal exposure to chemicals on the functional development to the brain in the offspring. Cancer Causes and Control. 8, 524-8.
  7. Garcia,A., Benavides,F., Fletcher,T. and Orts,E. (1998). Paternal exposure to pesticides and congenital malformations. Scand J Work Environ Health 24, 473-80.
  8. Watanabe, T and Sano, T. 1998. Neurological effects of glufosinate poisoning with a brief review. Human & Experimental Toxicology 17. 35-9.
  9. Cox, C. (1996). Herbicide Factsheet. Glufosinate. J. Pesticide Reform 16, 15-9.
  10. Ahn YJ, Kim YJ, Yoo JK . Toxicity of the herbicide glufosinate-ammonium to predatory insects and mites of Tetranychus urticae (Acari: Tetranychidae) under laboratory conditions.J Econ Entomol 2001, 94(1),157-61.
  11. Kutlesa NJ, Caveney S. Insecticidal activity of glufosinate through glutamine depletion in a caterpillar. Pest Manag Sci 2001 Jan;57(1):25-32.
  12. Hall L, Topinka K, Huffman J, Davis L, and Good A. Pollen flow between herbicide-resistant Brassica napus is the cause of multiple-resistant B. napus volunteers. Weed Science 2000, 48, 688-94.
  13. Orson J. Gene stacking in herbicide tolerant oilseed rape: lessons from the North American experience. English Nature Research Reports no. 443, English Nature, Jan. 2002, ISSN 0967-876X
  14. Ho MW. Chardon LL Public Hearing Ocober 26 2000 on behalf of Burnham Group, also in transcript
  15. Ho MW. Genetic Engineering Dream or Nightmare? Gateway, Gill & Macmillan, Bath and Dublin, 1998, 1999, Chapter on Perils amid Promises of Genetically Engineered Foods.
  16. Ho MW, Ryan A, Cummins J and Traavik T. Slipping Through the Regulatory Net: ‘Naked’ and ‘Free’ Nucleic Acids, Third World Network Biotechnology Series, Third World Network, Penang 2001.
  17. Guidance on best practice for the presentation of molecular data in submissions to the advisory committee on releases to the environment. Advice for applicants seeking permission to deliberately release genetically modified organisms into the environment (under Directive 2001/18/EC); see "Watering down EU’s new rules" by Mae-Wan Ho, Science in Society (formerly ISIS News) 13/14, February 2002, Institute of Science in Society, London.
  18. Ho MW and Steinbrecher RA. Fatal flaws in food safety assessment: critique of the joint FAO/WHO Biotechnology and Food Safety Report. Environmental & Nutritional Interactions 1998, 2, 51-84.
  19. Principles of gene manipulation, by Old and Primrose, Blackwell Science, 5th ed, 1994.
  20. DeVries J, Meier P and Wackernagel W. The natural transformation of the soil bacteria Pseudomonas stutzeri and Acinetobacter sp. by transgenic plant DNA strictly depends on homologous sequences in the recipient cells. FEMS Microbiology Letters 2001, 195, 211-5.
  21. Kumar S and Fladung M. Transgene repeats in aspen: molecular characterisation suggests simultaneous integration of independent T-DNAs into receptive hotspots in the host genome. Mol Gen. Gent 2000, 264, 20-8.
  22. Miller DG, Rutledge EA and Russell DW. Chromosomal effects of adeno-associated virus vector integration. Nature genetics 2002, 30, 147-8.
  23. Kumpatla SP, Chandrasekharan MB, Iyer LM, Li G and Hall TC. Genome intruder scanning and modulation systems and transgene silencing. Trends in Plant Sciences 1998, 3, 96-104.
  24. Horvath H, Jensen L,Wong O, Kohl E, Ullrich S, Cochran J, Kannangara C, and von Wettstein D. Stability of transgene expression, field performance and recombination breeding of transformed barley lines, Theor Appl Genet. 2001,1-11.
  25. Svitashev S, Ananiev E, Pawlowski WP, and Somers DA. Association of transgene integration sites with chromosome rearrangements in hexaploid oat. Theoretical and Applied Genetics 2000, 100,: 872-80.
  26. Tax FE and Vernon DM. T-DNA-associated duplication/transloations in Arabidopsis. Implications for mutant analysis and functional genomics. Plant Physiology 2001, 126, 1527-38.
  27. Windels P, Taverniers I, Depicker A, Van Bockstaele E and De Loose M. Characterisation of the Roundup Ready soybean insert. Eur Food Res Technol 2001, DOI 10.1007/ s002170100336, © Springer-Verlag; see also "Scrambled genome of Roundup Ready soya" by Mae-Wan Ho, ISIS Reprints on Transgenic Instability, ISIS Publications, ISIS, London March 2002.
  28. Ho MW, Ryan A and Cummins J. Cauliflower mosaic viral promoter - a recipe for Disaster? Microbial Ecology in Health and Disease 1999 11, 194-7.
  29. Ho MW, Ryan A and Cummins J. Hazards of transgenic plants with the cauliflower mosaic viral promoter. Microbial Ecology in Health and Disease 2000, 12, 6-11.
  30. Ho MW, Ryan A and Cummins J. CaMV 35S promoter fragmentation hotspot confirmed and it is active in animals. Microbial Ecology in Health and Disease 2000, 12, 189.
  31. Christou P, Kohli A, Stoger E, Twyman RM, Agrawal P, Gu X. Xiong J, Wegel E, Keen D, Tuck H, Wright M, Abranches R and Shaw P. Transgenic plants: a tool for fundamental genomics research. John Innes Centre & Sainsbury Laboratory Annual Report 1999/2000, p. 29. See "Top research centre admits GM failure" Transgenic Instability, ISIS Reprints, ISIS Publications, London, March 2002.
  32. Quist D and Chapela IH. Transgenic DNA introgressed into traditional maize landraces in Oaxaca, Mexico. Nature 2001, 414, 541-3, 2001.
  33. "Transgenic pollution by horizontal gene transfer?" by Mae-Wan Ho, Horizontal Gene Transfer, ISIS Publications, ISIS, London March 2002.
  34. Letter from Graeme Hunter, Scottish Executive, 17 August 2001.
  35. See "GM maize approve on bad science - report of ACRE public hearing on T25" by Mae-Wan Ho, 26 February 2002
  36. Gebbard, F. and Smalla, K. (1999). Monitoring field releases of genetically modified sugar beets for persistence of transgenic plant DNA and horizontal gene transfer. FEMS Microbiology Ecology 28, 261-72.
  37. "Horizontal gene transfer happens. A practical exercise in applying the precautionary principle" by Mae Wan Ho in Horizontal Gene Transfer, ISIS Reprints, ISIS Publications, London, March 2002.
  38. Pearce F. Desert harvest. New Scientist 2001, 27 October, 44-7.

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