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Sent: 20 June 2002 09:51
Subject: 60: Homologous recombination and gene replacement in plants
My name is Berthold Heinze. I am a research scientist in the Austrian Federal Office and Research Centre for Forests - Genetics Department, Vienna, Austria.
I would like to correct a statement that was made in this conference by Prof. Cummins (message 56, June 18): "All of the transgenic plants now commercialised or being tested, originated from genetic transformation based on illegitimate (non-homologous) recombination".
It gives a wrong impression. The following references report homologous recombination in plants. I also include an excerpt of an abstract of one of those:
- Carrer, H. and Maliga, P. Targeted insertion of foreign genes into the
tobacco plastid genome without physical linkage to the selectable marker
gene. BioTechnology [later became Nature Biotechnology] 13, 791-794. 1995.
- Morton, R. and Hooykas, P. J. J. Gene replacement. Molecular Breeding 1, 123-132. 1995.
Dix, P. J. and Kavanagh, T. A. Transforming the plastome: Genetic markers
and DNA delivery systems. Euphytica 85, 29-34. 1995.
Excerpt from the abstract:
Stable chloroplast transformants were first obtained following particle bombardment of tobacco leaves, and later by PEG-mediated uptake of DNA by protoplasts. The transforming DNA in these studies was itself of plastid origin and carried double (streptomycin, spectinomycin) antibiotic resistance which was used to select transformants. Integration was by homologous recombination, and both donor and recipient were Nicotiana species. Recent characterisation of plastid mutants of Solanum nigrum has allowed the extension of this gene replacement approach to include NicotianaSolanum combinations. The introduction of functional heterologous genes into the plastome is an alternative approach based on the use of constructs in which a bacterial resistance gene is flanked by sequences homologous to a region of the recipient plastome. Thus homologous recombination in the flanking sequences allows introduction of a foreign gene.
Kumar and Fladung [2001, referred to in message 56...Moderator] may have missed this in their Trends in Plant Science review paper (the papers above are not cited by them), maybe they were only referring to nuclear genes. However, genetic transformation can also affect chloroplast and mitochondrial genomes, as is nicely shown in the papers cited above.
Institute of Forest Genetics
Austrian Federal Office and Research Centre for Forests
Tel. +43 1 87838-2219 Fax -2250
e-mail: Berthold.Heinze (at) fbva.bmlf.gv.at
http://fbva.forvie.ac.at/db/personen.anzeige?person_id_in=1 changing pictures frequently - please call back!
Sent: 20 June 2002 10:03
Subject: 61: Re: gene flow risk assessment - plants
My name is Alan Raybould and I work for Syngenta. Before joining Syngenta, I was an ecologist in a public sector research institute in the UK.
I would like to comment on a point raised by Tom Nickson (message 24, June 7) and the response of Peter Jenkins (message 27, June 8). Tom described many of the suggested hazards of releasing transgenic plants as 'inoperative in terms of science based hypothesis testing'. [The hazards described by Tom Nickson in the 3rd-last paragraph of message 24 were "hazards associated with gene flow from GM crops such as: impacts on biodiversity, impacts on population dynamics, genetic swamping, and alterations of gene pools"...Moderator]. Peter thought that this was too broad, and what Tom had identified were the difficulties of scaling up from field trials to commercial-scale releases of GM crops.
I think Tom identified something more than problems of scale up. A scientific term is operational if most people can agree on which variables represent the phenomenon being studied. Tom's list includes several phenomena that are not operational because we are not agreed on the variables that specify them. Unless we can agree on the changes in measurable variables that constitute 'genetic swamping', 'impacts on biodiversity', 'alterations of gene pools' etc., even very large experiments will fail to advance scientific risk assessment.
The lack of operational end points is a serious problem for ecologists. In the short term, we can justify our existence to regulators, industry and the general public because we are seen to be collecting data that are essential for the risk assessment process. However, the process of collecting data is not an end in itself. Eventually we must produce quantitative predictions about how agreed variables will change after the release of a GM plant. If we fail to do this, ecologists will rightly be dismissed as having nothing scientific to offer GM risk assessment.
Jealott's Hill International Research Centre
Berkshire RG42 6EY
alan.raybould (at) syngenta.com
direct line: +44 (0) 1344 414620
fax: +44 (0) 1344 413688
Sent: 20 June 2002 10:24
Subject: 62: Re: gene flow risk assessment - plants
This is Tom Nickson (Monsanto Co. in St. Louis, United States) responding to comments from Joe Cummins (message 12, June 5) and Peter Jenkins (message 27, June 8).
Both Peter and Joe cited volunteer canola with multiple tolerances produced under field conditions as evidence of "risk" associated with transgenic herbicide tolerant canola. Further, Peter noted that this observation is inconsistent with my comment that "the current biotech products have shown no measurable risks compared to the risks already present from their traditionally grown counterparts" (message 24, June 7).
I encourage the participants of this conference who wish to critically evaluate this matter to carefully read the authoritative paper: Hall, L. Topinka, K.; Huffman, J.; Davis, L.; Good, A. 2000. Pollen flow between herbicide resistant Brassica napus is the cause of multiple-resistant B. napus volunteers. Weed Science, vol. 48, 688-694.
While the authors clearly state that herbicide resistant Brassica napus (canola in Canada) "has raised several weed management concerns", they also state: "The introduction of herbicide-resistant B. napus has offered producers a variety of new, safe and effective strategies for weed control. Despite rapid adoption, agronomic tribulations have been predictable and minor.". Hall et al. also note that the "circumstances leading to the discovery of cross-resistant volunteer B. napus were atypical" citing the producers' practices. If one reads a bit further, these authors acknowledge the common nature of gene flow and high probability of the formation of progeny with multiple tolerances; to which I add that this will be a function of acreage and spatial proximity of the different herbicide tolerant varieties. However, given that this study constituted one grower in Alberta, and that over 50% of the canola grown in Canada has been herbicide tolerant for the last 3 years, Hall et. al. state, "The lack of multiple resistant volunteers suggests multiple-resistant B. napus volunteers are being controlled by chemical and nonchemical management strategies and are therefore not an agronomic concern to most producers."
Part of the argument put forth by the Royal Society of Canada and cited by Peter is illogical. Specifically, " "gene stacking" represents a serious development because,....,farmers are forced to use older herbicides, some of which are less environmentally benign than newer products" is very odd. The older herbicides are the ones that farmers had available prior to the introduction of herbicide tolerant crops, and the newer environmentally superior products are those that are now possible to use because of genetic modification. I interpret the current situation as beneficial to both farmers in Canada and the environment. The farmers now have more tools to produce canola than they had prior to GM, and these tools are more environmentally benign. It is now a matter of good stewardship on the part of industry, academia and farmers to use this new technology sustainably.
Based on the available evidence and scientific fact and the expert opinion of those who have published scholarly works on this matter, I submit that this example does not constitute a measurable ecological risk. Rather, it is a good example of how agricultural systems have to adapt to new technology. New information is obtained based on observation followed by scientific inquiry as evident by the paper in Weed Science cited above.
Thomas E. Nickson, Ph.D.
Ecological Technology Center
Monsanto Company, V2B
800 N. Lindbergh Blvd.
St. Louis, MO 63141 USA
thomas.nickson (at) monsanto.com
Sent: 20 June 2002 11:40
Subject: 63: Re: Evolutionary risks of transgenes
[The discussion seems to be drifting away from the theme of this conference, which is the potential importance and impact of gene flow from genetically modified (GM) crops, forest trees, fish or animals to non-GM populations, with particular focus on developing countries. Thus, for example, differences between transgenes and genetic changes through conventional or natural selection per se should not be the focus, but rather the impacts or relevance of such differences on gene flow....Moderator]
This is from Dr Wayne Knibb. I am a geneticist (population and molecular biologist) working on aquacultured species.
I am trying to reconcile the two comments of Bill Muir (message 34, June 10) 1) "but I do not think that risk [of GM plants or animals to genetic variability within species...Moderator] is any greater than with domestic breeding" and 2) "A transgene should be thought of as a mega-mutation, and nothing more" [These 2 quotations are from the last and fifth paragraphs respectively of Bill Muir's message...Moderator], with those of Muir (message 57, June 19): "Secondly, extrapolation of natural mutation rates with associated environmental harms to engineered mutations and possible associated harms is not scientifically valid for a number of reasons...."
Muir seems to accept that there are risks from natural genetic processes. This advances the debate to one of relative risks. Muir embraces the (presently) speculative perspective that genetic engineering engenders extra risk. (Incidentally, Muir may have misread my message 51 (June 17). Using the scallop example, I posed the question not of equivalence but of negligible risk of genetic engineering compared with classical genetic changes, hence Muir's analogy with radon gas may be inappropriate in logic, and in biology).
Also, for balance, possibly scientific accuracy, I'd like to list the
following points from the published literature that are somewhat at variance
with Muir's perspectives of message 57:
1. There are no empirical data showing new species formation by genetic engineering.
2. Non-point mutations (translocations, transpositions) are common (and arguably pose orders of magnitude more risk than genetic engineering).
3. Point mutations can generate very large phenotypic changes - i.e. changes more dramatic than those conceivable from genetic engineering, such as a second set of wings in Drosophila. Indeed nature has put "wings" on fish and we shouldn't underestimate the potential and flexibility of natural genetic processes. Conversely, natural processes can manipulate whole genomes through ploidy, hybridisation and even genome "fusion" with mitochondrial and nuclear DNA.
4. The fitness of phenotypic change is inversely proportional to the magnitude of the change, not vice versa as suggested by Muir (see Knibb 1997, 2002).
5. There is no empirical evidence that genetically engineered changes are more likely (than natural mutations) to be fit in the wild. We have no knowledge of the blueprint or architecture of fitness of species, and without this knowledge any changes we make, no matter how deliberate in our minds, will be accidental with respect to fitness - i.e. one may have a perfectly fine and well designed spanner, but if you don't have the blueprint to say, a power plant, the chance of improving electrical output (read fitness) by random tinkering is negligible. This explains why we've failed in the past (in insect control programs) to deliberately construct classical changes with fitness advantages in the wild.
6. Issues of process (method and type of genetic change) and form (phenotype), and their similarities/differences between engineering and classical changes are quite secondary to the critical and central issue of wild fitness. Because of pleiotropy, genetic changes, however they are made, and whatever phenotypic class of change (notwithstanding neutral mutations), are likely to reduce wild fitness.
Such issues can be debated to and fro, and to break this cycle I attempted to establish a formal testable (i.e. scientific) hypothesis of negligible environmental risk from GMOs (Knibb 1994, 1997). It is for the scientific community to assess whether this hypothesis was falsified over the last decade using empirical data (setting aside hypothetical speculation). If not falsified, at some point (in 1, 10, 20 years?) this hypothesis should become dogma and guide regulators.
Knibb, W.R. 1994. Genetic improvement of warmwater fish and their
environmental impact. 3rd International Marine Biotechnology Conference:
Book of Abstracts, Tromsoe University. p 90.
Knibb, W. R. 1997. Risk from genetically engineered and modified marine fish. Transgenic Research. 6:59-67.
Knibb, W. R. 2002. Ecological risk from aquatic LMOs. Proceedings from "LMOs and the Environment: An International Conference". Raleigh-Durham, the United States, 27-30 November 2001. In press. (please contact author for copies)
Dr Wayne Knibb
Principal Research Scientist
Bribie Island Aquaculture Research Centre
144 North Street, Woorim
PO Box 2066
Bribie Island Queensland 4507
Ph (07) 34002000 / 2052
e-mail: wayne.knibb (at) dpi.qld.gov.au