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"Cauliflower mosaic virus recombination , when and where?"

by Prof Joe Cummins


Cauliflower mosaic virus (CaMV) promoter gene is used in essentially all of the commercially released genetically modified (GM) crops. The gene is needed because it drives the production of gene messages from the genes inserted to provide herbicide tolerance, insect resistance, antibiotic resistance or a range of functions deemed to improve the commercial quality of the crop. In the absence of the promoter gene the inserted genes remain inactive, while in its presence the gene activity is maintained at a high level in all of the plant tissues, with little interference from changing environmental conditions that effect the activity of promoters native to the crop plant.

The CaMV promoter gene has been found to be a "hot spot" for recombination leading to exchange of gene sequences at elevated frequency (Ho et al Microbial Ecology in Health and Disease (no.4,1999).. Such exchanges may include sequences from neighboring genes on the crop plant chromosome or genes on other chromosomes. The latter exchanges produce translocations and deletions in the chromosomes. Recombination can produce unpredictable and potentially devastating gene arrangements.

For example, a growing body of evidence shows that plant DNA viruses may recombine to produce virus that attack animals or plant virus may be acquired from bacteria. It not yet clearly established as to the extent and frequency of such exchanges in contemporary time, however, it is clear that the specific virus diseases have only recently been described. For example, a pig wasting disease of growing concern has been found to have been caused by a virus that originated from clover, coconut or banana (Meehan, et.al. J. Gen. Virol. 78,221-7,1997). Presently it is yet unclear when the virus jumped from plant to pig or whether or not the plant virus may continue to generate recombinants infecting animals. In this regard, it is worth pointing out that HIV sequences function rather well in the CaMV promoter (Noad et al John lnnes Centre & Sainsbury Laboratory Annual Report 1998/99).Many advocates of GM crops claim that safety of the CaMV promoter is assured by the presence of CaMV in cabbage and other crucifers is assured by the fact that animals including humans have consumed virus infected plants for a long time. However, such 'authorities' fail to note that plant and animal pararetrovirus have a common origin and little effort has been made to find plant pararetrovirus DNA sequences of contemporary origin in animal pararetrovirus or in endogenous retrotransposon sequences. Even with those limitations it is very clear, as discussed below, that recombination has significantly different features in CaMV replication than it does in CaMV genes integrated into the chromosome.

The CaMV gene integrated into chromosome is influenced by both meiotic recombination and by mitotic recombination and by meotic and mitotic gene conversion. Localization of those genes in the nucleus provides a rich source of DNA for exchange and that DNA is highly variable in sequence.

When CaMV (the infecting virus) infects the plant cell it forms a circular minichromosome in the plant cell nucleus. That minichromosme transcribes many RNA copies of one of its DNA strands driven by the CaMV promoter.

The RNA strands are transported to the cytoplasm were they construct enzymes and structural proteins for their replication. The replication of each RNA strand to make the circular DNA chromosome of the virus includes reverse transcription of the RNA strand to make a DNA chromosome strand, as the reverse transcription proceeds RNase H removes the newly copied RNA strand while DNA polymerase replaces the RNA strand to make the finished circular chromosome. Recombination is very active , particularly near the origin of replication, but so long as only identical copies of the viral minichromosome are available for recombination the recombinants are also identical. Recombination does not yield variability in this progeny.

However, co-infection with different virus strains will yield recombinants, but such co-infection is not commonplace outside the laboratory.

What I am saying is that viral genes introduced into the host chromosome are subject to high level recombination and gene conversion while the normal cytoplasmic replication of virus is from a uniform group of molecules whose exchange ( recombination) does not yield variability. The most significant risks of genetic engineering remains the recombination of genes to create new and unpredictable variants that can spread rapidly, as in the virus, because the biological system is ill prepared to cope with the recombinant. What seems to have happened is that the 'experts' who dwell upon the consumption of virus in crops that are not genetically engineered have neglected the fact that the recombinants from genetically engineered crops are entirely different from virus replicated in GM free crops.

Somewhat shockingly, the bureaucratic risk evaluators in the United States based their evaluations on that rather elementary error. Sadly, those evaluators also seem to have turned a blind eye to the risk of recombination leading to infection of animals with virus of plant origin or for that matter infection of plants with virus of bacterial origin. These phenomena are well described in the literature of science.

I have not been shocked by the "experts" who glibly ridicule those who deal with the serious issues of genetic recombination, they seem interested only , in winning, at any cost. However, I am very shocked at the 'authorities' who try to prevent publication of articles that disagree with their mistaken views. The groundless and intemperate threats of such 'experts' makes me think that they may very well be sliding the slippery slope that the geneticist, Dr.Dr. Josef Mengele fell.

e-mail: jcummins@julian.uwo.ca

 


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