[Pil-pc-oceania] gm

Wed Mar 12 17:07:53 EST 2008

The Best Kept Secret of GM Crops
Witness Statement to ACRE
http://www.i-sis.org.uk/secretGMcrops.php
For ACRE open hearing on the criticisms of T25 GM maize risk assessment

The hearing will take place from 10.00am to 2.00pm on Wednesday, 20
February, in Room 7A, B and C, Ashdown House, Department for
 Environment, Food and Rural Affairs, 123 Victoria Street, London SW1E 6DE.

Dr. Mae-Wan Ho

Institute of Science in Society, PO Box 32097, London NW1 0XR, UK

I am speaking against the market approval of T25 because there is no
 evidence that it is a genetically stable, uniform line, the single most
 important criterion for approval. For unless it is genetically stable,
 you might as well forget about environmental or health risk assessment.
 And genetic instability is also a serious safety issue. 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
 [1].

The new EC Directive on deliberate release 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.

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 [2,3]. 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’s referred to as horizontal gene transfer and recombination.
 Transgenic DNA can spread to every species that interact 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 occur [4]. 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 [5], which is
 derisory. We need data for at least five successive generations [6]. No
 such data have come forward from the companies. On the contrary,
 companies have been allowed to hide under ‘commercial confidentiality’.

I am putting to you twelve reasons why trangenic DNA is different from
 natural DNA, and is more likely to spread by horizontal gene transfer
 and recombination, both by design and otherwise. I hope you will refute
 these point by point.

(The details are in two ISIS reprint collections on transgenic
 instability and horizontal gene transfer that I am presenting to ACRE, for
 free.)

    * All artificial constructs tend to be unstable, so much so that
 this is a topic in a standard text-book on genetic engineering [7].
 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 [8].
    * 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 [9] and the human genome [10]. 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 [11].
    * 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 [12-14]
 leading to chromosomal rearrangements, genome scrambling, in other words.

    * Monsanto’s Roundup Ready soya, commercially grown for years, was
 finally analysed by molecular methods. 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 [15]. All very different from the original data
 provided by Monsanto.

    * Recombination hotspots within the transgenic DNA, 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 [16-18], and demanded that 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 [19], 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 [20]. Molecular analysis showed that the sequences next
 to the promoter are very diverse, as consistent with horizontal gene
 transfer and recombination [21].
    * CaMV 35S promoter is active in species across the entire living
 world, including frog eggs and human cells [18], 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 [4]. 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 [5].
    * Transgenic DNA from GM plants was found to transfer to soil
 bacteria. The possibility of transfer to bacteria in the mouth and gut of
 animals was suggested in laboratory investigations funded by the UK
 government. There is also evidence suggesting that transgenic DNA from crop
 plants has transferred to soil bacteria in the field [22]. But ACRE has
 ignored that by a selective interpretation of the scientific evidence
 that seems to me contrary to both the precautionary principle and good
 science [23]. 

In summary, there is no reason to believe T25 is stable. Furthermore,
 it has especially hazardous sequences, including the CaMV 35S promoter
 and an ampicillin resistance gene that, though inactive, can easily be
 transferred into integrons that will provide it with a promoter to make
 it functional [1]. T25 has uncharacterised sequences that might be
 involved in causing diseases. Finally, it has an origin of replication,
 which enables the transgenic DNA to be replicated as a plasmid if
 transferred into bacteria, thereby greatly increasing horizontal gene transfer
 on to other species. The origin of replication is also a recombination
 hotspot, and there have been strong recommendations from a recent joint
 FAO/WHO Expert Consultation on Foods Derived from Biotechnology that
 transgenic lines containing this sequence should not be approved on
 safety grounds [24].

   1. Ho MW. Chardon LL Public Hearing Ocober 26 2000 on behalf of
 Burnham Group, also in transcript.
   2. See Ho MW. Genetic Engineering Dream or Nightmare? Gateway, Gill
 & Macmillan, Bath and Dublin, 1998, 1999, Chapter on Perils amid
 Promises of Genetically Engineered Foods.
   3. ISIS Reprints on Transgenic Instability, 1999-2001, ISIS
 Publications, London.
   4. 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.
   5. See Watering down EC Directive on Deliberate Release ISIS Report,
 February 2002.
   6. 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.
   7. ISIS Reprints on Horizontal Gene Transfer, 1999-2001, ISIS
 Publications, London.
   8. Principles of gene manipulation, by Old and Primrose, Blackwell
 Science, 5th ed, 1994.
   9. 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.
  10. Kumar S and Fladung M. 2000. 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.
  11. Miller DG, Rutledge EA and Russell DW. Chromosomal effects of
 adeno-associated virus vector integration. Nature genetics 2002, 30,
 147-8.
  12. Kumpatla, S.P., Chandrasekharan, M.B., Iyer, L.M., Li, G. and
 Hall, T.C. (1998). Genome intruder scanning and modulation systems and
 transgene silencing. Trends in Plant Sciences 3, 96-104.
  13. 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.
  14. Svitashev S, Ananiev E, Pawlowski WP, and Somers DA. 2000.
 Association of transgene integration sites with chromosome rearrangements in
 hexaploid oat. Theoretical and Applied Genetics 2000, 100,: 872-80.
  15. Tax FE and Vernon DM. T-DNA-associated duplication/transloations
 in Arabidopsis. Implications for mutant nanalysis and functional
 genomics. Plant Physiology 2001, 126, 1527-38.
  16. Windels P, Taverniers I, Depicker A, Van Bockstaele E and De
 Loose M (2001). Characterisation of the Roundup Ready soybean insert. Eur
 Food Res Technol DOI 10.1007/ s002170100336, © Springer-Verlag; see also
 "Scrambled genome of Roundup Ready soya" by Mae-Wan Ho, ISIS Reprints
 on Transgenic Instability, 1999-2001, ISIS Publications, London.
  17. Ho MW, Ryan A and Cummins J. Cauliflower mosaic viral promoter –
 a recipe for Disaster? Microbial Ecology in Health and Disease 1999:
 11: 194-197.
  18. 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.
  19. Ho MW, Ryan A and Cummins J. CaMV35S promoter fragmentation
 hotspot confirmed and it is active in animals. Microbial Ecology in Health
 and Disease 2000: 12: 189.
  20. 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" ISIS Reprints on Transgenic Instability,
 1999-2001, ISIS Publications, London.
  21. Quist D and Chapela IH. Transgenic DNA introgressed into
 traditional maize landraces in Oaxaca, Mexico. Nature 2001, 414, 541-3, 2001.
  22. "Transgenic pollution by horizontal gene transfer?" by Mae-Wan
 Ho, in ISIS Reprints on Horizontal Gene Transfer, 1999-2001, ISIS
 Publications, London.
  23. "Horizontal gene transfer happens. A practical exercise in
 applying the precautionary principle" by Mae Wan Ho in ISIS Reprints on
 Horizontal Gene Transfer, 1999-2001, ISIS Publications, London.
  24. Joint FAO/WHO Expert Consultation on Foods Derived from
 Biotechnology, WHO Headquarter, Geneva, September 24-28, 2001. 

martin

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