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  • From: "Tradingpost" <tradingpost@lobo.net>
  • To: livingontheland@lists.ibiblio.org
  • Subject: [Livingontheland] The Best Kept Secret of GM Crops
  • Date: Tue, 11 Mar 2008 19:09:18 -0600

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.







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