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After Monsanto’s GM Meltdown in the USA…

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Resistance to certain insects in GMO crops produces a wonderful opportunity for other pests to take their place, and they are rapidly doing so. More and more toxic insecticides and “death-gene”  technologies are being ramped up to address the problem- which shouldn’t have been created in the first place.

Institute for Science in Society April 14, 2010    Prof. Joe Cummins

Syngenta comes to the rescue to keep the transgenic treadmill going

One major impact of crops genetically modified (GM) for insect resistance is that the Bacillus thuringiensis (Bt) Cry toxins conferring insect resistance are specific for particular pests. After the Bt crops have been planted for several years, the target pest is usually diminished, leaving an ecological niche into which another insect pest species may invade. This has already happened with Bt cotton in India [1] (Mealy Bug Plagues Bt Cotton in India and Pakistan, SiS 45) and in the United Stated, where the tarnished plant bug has emerged as the major pest in the cotton belt [2] (GM Crops Facing Meltdown in the USA, SiS 46).

Now Christoph Then of Test Biotech, an independent German research group, reports on the spread of the western bean cutworm (Striacosta albicosta) and the massive damage inflicted on Bt maize in the United States [3]: “The infestation has been observed since the year 2000.…. This cutworm has historically been confined to very limited regions and did not cause any major problems in maize crops. For several years now the pest has been spreading into more and more regions within the US Corn Belt and causing substantial economic damage. In 2009, maize plants affected by the western bean cutworm were even found in Canada for the first time. According to scientific publications, this new pest has been caused by the large-scale cultivation of genetically engineered plants expressing Cry1Ab such as MON810. It is seen as a case of ‘pest replacement’, often found where there is extensive use of pesticides in industrial agriculture. Pest replacement means that new ecological niches open up which other competitors then occupy. In this case, a naturally occurring competitor of the western bean cutworm has been intentionally suppressed by the extensive cultivation of Bt maize plants, thus allowing the new pest to spread on a large scale and heavily infest the crop. A whole arsenal of insecticides – some of them highly toxic – and genetically engineered multi-stacked maize are recommended for controlling the pest.”

Syngenta MIR162 to the rescue

For the most part, the pesticides used to combat new pests are toxic, expensive and leave residues on food and feed.  The Bt Cry toxins available for genetic modification have not proven   sufficiently effective against the newly emerged pest. Syngenta Corporation was quick to fill the pesticide gap by introducing a maize line called Agrisure Viptera to control western bean cutworm.  That GM maize line is derived from event MIR162 incorporating a Bt vegetative insecticidal protein, VIP3Aa [4]. VIP toxins are produced in growing Bt cells as distinct from the Cry toxins that are produced as crystals in stationary stage sporulating Bt cells. Agrisure Viptera was cleared for commercial release by USDA/APHIS and USEPA in time for the growing season in 2010.

Event MIR162’s Bt insecticidal vegetative protein gene vip3Aa20 is driven by a maize polyubiquitin promoter with the CaMV 35S 3’ polyadenylation termination signal. A selectable marker pmi encoding mannose-6-phosphate isomerise from E. coli, also driven by the maize polyubiquitin promoter, with Agrobacterium nopaline synthase terminator. The phosphomannose-isomerase converts mannose-6-phosphate to fructose-6-phosphate. Only transformed cells are capable of utilizing mannose as a carbon source. Transgenic plants regenerated from selected transformed immature embryo-derived calli contained the pmi gene and the gene was transmitted to the progeny in ‘Mendelian’ fashion [6]. (This is based on the statistical misuse of failure to depart from ‘Mendelian ratios’ as evidence of transgene stability,  as pointed out by ISIS [7] GM Rice Unstable (isisnews 9/10). The Syngenta petition for non-regulated status of MIR162 maize was an extensive document describing the construction of the transgenic maize line and its field testing for productivity and resistance to pests. VIP3Aa20 produces pores in the gut cell membrane of insect pests that caused the cells to burst; its target cell proteins are different from those of the Cry proteins. The impact of MIR163 on non target organisms were examined, but only with the VIP3Aa20 protein produced in the bacterium E coli, which is  different from that expressed in the transgenic maize.  The latter is transcribed from a DNA sequence that had been altered to optimise production of VIP3Aa20 protein in maize, differing by several amino acids, but assumed, unjustifiably, to be insignificant [6].

In 2005, USDA/APHIS  determined that Syngenta Corporation cotton event COT102 with transgene VIP3A was no longer regulated, and is now used to control a number of Lepidopteron pests  [8, 9].

Syngenta’s patented death proteins

Syngenta corporation, producer of chemical and biological pesticides, has patented the vip genes for use in transgenic crop plants and microbes [10]. The patent provided evidence that Vip3A toxin produces apoptotic cell death, a series of cytological changes including the production of membrane bound apoptotic bodies and activation of endonuclease enzymes that cleave chromatin into discrete fragments. Apoptosis (meaning petals falling from a flower) or programmed cell death, is common to all cells with discrete nuclei. Apoptosis is a part of normal development, but that induced by VIPp3A toxin is not. In order to function fully in the plant cells the vip3A gene is modified in its coding sequence, and is given additional extraneous sequences: a strong promoter to drive transcription, an intron to facilitate transfer of the pre-messenger RNA from nucleus to cytoplasm, a transcription terminator, and signal for polyA addition. The insect VIP3A receptor was identified and its ‘death domain’ recognition sequence characterized. Organisms whose cells have nuclei generally have families of receptors with ‘death domain’ recognition sequences, just as the insect VIP3A receptor is a unique member of a family of receptors [11, 12]. The death domain of VIP proteins is a 60 to 70 amino-acid motif, that is present in many proteins and phylogenetically conserved, as I pointed out previously [13] (Death Domains in New Bio-pesticides, SiS 26). The effects of VIP proteins on non-target organisms need to be very thoroughly investigated. USDA /APHIS finding of no significant impact (FONSI) has allowed the unconfined cultivation and use of COT102. The environmental assessment responded to public comment about apoptosis,  but did not discuss the topic extensively [12].

Continuing transgenic treadmill

Syngnta seems to have quickly turned adversity into opportunity. Nevertheless, once the western bean cutworm occupied niche is subdued, another resistant pest will appear to provide further opportunity for enriching biotech corporations in the endless transgenic treadmill [14] (see Glyphosate Resistance in Weeds – The Transgenic Treadmill, SiS 46).

The only escape from the transgenic meltdown may well be organic cropping [2].

Posted with permission.

A fully referenced version of this article is posted on ISIS members’ website and can be downloaded here

See also

Bayer admits GMO contamination out of control

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2 Responses

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  1. ishtarmuz

    May 25, 2010 at 5:54 pm

  2. […] You also might like: After Monsanto’s GM Meltdown in the USA […]


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