5.3—Transgenes are destroyed in the gut
Transgenes do not have special mechanisms that allow them to survive in the gut over the long-term
See Genetic Roulette’s False Claims at Bottom of Page
Analysis of Peer-Reviewed Research:
In this section Jeffrey Smith makes several misleading claims to support his supposition that transgenes from plants can take up permanent residence in gut bacteria. He wrongly claims that the 35S promoter used to drive some transgenes in genetically engineered plants will give a unique advantage to plant genes and enable them to be expressed in bacteria in the gut. Smith seems unaware that there are numerous promoters similar to 35S in many different plants, so this remote possibility already occurs with conventional foods. He also speculates about the herbicide tolerant genes from plants becoming established in gut bacteria, but this is completely unrealistic because miniscule herbicide concentrations in the gut will not select for herbicide tolerant bacteria. His idea that antibiotic markers from transgenic plants will provide transgenes with ability to permanently reside in the gut should be assessed against the already very high frequency of antibiotic resistance in the existing gut microbial flora. Smith is so desperate to create the impression that transgenes have been detected in gut bacteria that to support his case, he relies on 8-year-old press reports that have never been worth mentioning as evidence of risk. These old stories have never been validated in the peer- reviewed scientific literature.
1. Absence of herbicide in the gut means that the herbicide resistance genes offer no selective advantage to bacteria. Genetic Roulette argues that genes conferring herbicide tolerance from transgenic plants could out allow bacteria capturing these genes to have a permanent advantage over the other gut bacteria. Fortunately, the part of herbicide treated plants we use as food — the seed — contains only a minute fraction of any herbicide residues that stay in the plant (Ruhland M and others 2004). Additionally, health regulations place limits on the amount of herbicide that can be present in food. Further dilution of the minute amounts of herbicide residues takes place when food is cooked and eaten as part of diets. Thus there is no effective concentration of herbicide present in the gut. The absence of herbicides in our gut means that bacteria that acquire the herbicide tolerance gene have no selective advantage, and would not be able to proliferate in the highly competitive environment of the gut.
2. Origins of replication cannot provide plant transgenes a mechanism to proliferate rapidly in the gut. Plasmids are small bacterial chromosomes used by genetic engineers to manipulate DNA and portions of plasmids have often been added to the genomes of genetically modified plants. This section of Genetic Roulette is concerned with the risk that plasmid DNA from genetically engineered plants may accidently get back into gut bacteria. To understand this issue, it important to remember that to be permanently carried in a strain of bacteria, a bacterial mini-chromosome (the plasmid) needs a DNA segment called the “origin of replication”. Without an origin of replication, the mini-chromosome cannot be transmitted permanently in a strain of bacteria.
Genetic Roulette argues that plant transgenes containing an origin of replication may help proliferation of transgenes in gut microbes. It explains that such sections of plasmids contained in the origins of replication that are used by the plasmids to proliferate permanently in microbial cells. However for this origin of replication to work in bacteria a circular form of DNA has to be regenerated from the transgene, and in plant cells the transgene does not exist as the circle. It is highly unlikely that the circle can reform. This provides a barrier against assembly of plasmids from plant transgenic DNA (Bennett and others 2004, Thomson 2001, van den Eede and others 2004). Many transgenic plants are constructed without the use of plasmids or plasmid origins of replication and have no capacity to proliferate in bacteria.
3. Transgenes are no more likely than other plant genes to function in bacterial DNA. Genetic Roulette argues that the cauliflower mosaic virus 35S promoter used to drive transgene expression can work in bacteria, and that this would provide a unique ability for genes coupled with this promoter to work in bacteria. Not so. As discussed in Section 2.5, there are numerous fragments of Cauliflower mosaic related viruses (with similar promoters) inserted into plant genomes, so the presence of the 35S promoter in transgene does not provide a unique possibility for plant genes to be active in bacteria, should the extremely rare event take place involving transfer of a plant gene to a gut bacterium occur as argued by Smith (Gayral and others 2008, Hansen and others 2005, Staginnus , Richert-Pöggeler 2006, Staginnus and others 2007).
4. Permanent colonization of the gut as imagined by Smith is highly unlikely. Continual flow of food through the gut ensures that colonization of the gut by bacteria is transient. Additional unused capabilities, such as new genes, would place a burden on the bacteria and special advantages are needed to overcome this burden. Biologists call this a “fitness cost.” A cell that wastes its resources using genes that aren’t needed will be selected against. This acts against permanent establishment of genetically altered bacteria in the gut.
5. Existing overuse of antibiotics is the main driving force for high numbers of antibiotic resistant bacteria being present in gut flora. For acquired transgenes to be retained by bacteria it is necessary for them to confer an advantage in the highly competitive gut environment. Antibiotic resistance genes from plants confer no new advantage on gut bacteria, because the gut bacteria already possess antibiotic resistance genes (Bennett and others 2004; Berche 1998; Calva and others1996).
6. No movement of a functioning transgene from plants to bacteria to bacteria has ever been reported in the peer-reviewed scientific literature. To add credibility to his arguments, Smith tries to create the impression that transgenes have been detected in gut bacteria but because no full-length working plant transgene has ever been properly described in the scientific literature as being transmitted to a bacterium, he has to rely on less trustworthy sources of information. In this section he resorts to citing newspaper and TV reports of supposed gene movement into bacteria from plants, but produces no genuine scientific publication. The May 2000 press comments by Professor H. H. Kaatz on gene fragments supposedly being detected in bee microbes have never been confirmed by peer-reviewed scientific papers. This claim is in fact only made by anti-GMO activists. Plant transgene movement to bacteria has never been verified.
See also
5.2. Genetically engineered plants do not promote movement of genes from plants to bacteria.
References
Bennett PM and others, Working Party of the British Society for Antimicrobial Chemotherapy (2004). An assessment of the risks associated with the use of antibiotic resistance genes in genetically modified plants: report of the Working Party of the British Society for Antimicrobial Chemotherapy. J Antimicrob Chemother. 2004 Mar;53(3):418-31. Epub 2004 Jan 28.”…the argument that occasional transfer of these particular resistance genes from GM plants to bacteria would pose an unacceptable risk to human or animal health has little substance. We conclude that the risk of transfer of AR genes from GM plants to bacteria is remote, and that the hazard arising from any such gene transfer is, at worst, slight.”
Berche P (1998) Les plantes transgéniques et la resistance aux antibiotiques. Méd Thérap 4:709–719
Calva, JJ, Sifuentes-Osornio J, Cer´on C (1996) Antimicrobial resistance in fecal flora: longitudinal community-based surveillance of children from urban Mexico. Antimicrob Agents Chemotherapy 40:1699–1702
Gayral P, Noa-Carrazana JC, Lescot M, Lheureux F, Lockhart BE, Matsumoto T, Piffanelli P and Iskra-Caruana ML (2008) A single Banana streak virus integration event in the banana genome as the origin of infectious endogenous pararetrovirus. J Virol. 82(13):6697-710.
Harper G, Hull R, Lockhart B, and Olszwski N, and others (2002). Review. Viral sequences integrated into plant genomes. Annual Review of Phytopathology 40:119–36. Numerous bits of viruses are found inside the chromosomes of plants that we eat.
Hansen CN, Harper G and Heslop-Harrison JS and others (2005). Characterisation of pararetrovirus-like sequences in the genome of potato (Solanum tuberosum). Cytogenet Genome Res. 2005;110(1-4):559-65.
Ruhland M, Engelhardt G and Pawlizki K (2004). Distribution and metabolism of D/L-, L- and D-glufosinate in transgenic, glufosinate tolerant crops of maize (Zea mays L ssp mays) and oilseed rape (Brassica napus L var napus). Pest Management Science 60: 691-696. Only a tiny fraction of herbicide gets into seeds.
Staginnus C and Richert-Pöggeler KR (2006) Endogenous pararetroviruses: two-faced travelers in the plant genome. Trends Plant Sci. 11(10):485-91.
Staginnus C, Gregor W, Mette MF, Teo CH, Borroto-Fernández EG, Machado ML, Matzke M and Schwarzacher T (2007) Endogenous pararetroviral sequences in tomato (Solanum lycopersicum) and related species. BMC Plant Biol. 7:24.
Thomson J (2001). Horizontal transfer of DNA from GM Crops to bacteria and to mammalian Cells. Journal of Food science 66(2):188-193.
1. Once transfer into gut bacteria, transgenes that confer survival advantages, allowing them to endure and spread.
2. These advantages may be due to antibiotics or herbicide resistance, promoters that function in bacteria and genetic mechanisms that promote uncontrolled replication.
3. Having “infected” our gut bacteria, the foreign genes and the proteins they create may be harmful.
Transgenes from plants, if incorporated into gut bacteria, may give advantages to the bacteria and allow them to proliferate over a long term in the gut, according to Genetic Roulette’s speculations.
