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More on Bt Resistance
Prof. Joe Cummins deals with further
intricacies on the supposed lack of Bt resistance outbreaks from commercial
growing of Bt crops.
The references for this article are available in the ISIS members site. Full details here
My report on the surprising finding that little genetic resistance has
been observed in transgenic crops containing transgenes for Bacillus
thuringiensis (Bt) toxin to kill insect predators [1] evoked response from
Bruce Tabashnik, a leading researcher in the new field of resistance management
[2]. I pointed out that there are a number of Bt toxin genes, each of which is
highly polymorphic (with many different variants), including some that are
synthetic so the absence of resistance breakouts could be related to the
diversity and polymorphism of transgenes in the crops, along with the United
States sanction of using pesticide sprays in the refuge areas, as both normal
susceptible pest and resistant mutants will be killed by the spray.
Tabashnik did not challenge my assertion that the pesticide spray will
destroy resistant mutants, but claims that the polymorphism of the transgenic
stocks was low, because, for example, most of the millions of acres transgenic
corn contain the Bt Cry1Ab gene while transgenic cotton has mainly the Cry1Ac
gene. So, the crops should be considered essentially monomorphic, thereby
providing a large target for resistance to evolve.
The presumption that transgenes described as Bt Cry1Ab in maize or Bt
Cry1Ac in cotton are nearly identical is fallacious. However, the products of
the mainly synthetic genes Cry1Ab toxin in maize and Cry1Ac toxin in cotton are
similar to the respective product of the natural gene is perhaps justified, but
they are not identical. More importantly, the various ways in which the genes
specify Cry1Ab or Cry1Ac are synthesized and altered from the natural gene are
described in the bio-pesticide registration documents of the Environmental
Protection Agency (EPA) [3-6], and the determination of non-regulated status
documents of the United States Department of Agriculture (USDA) [ 7-11].
The genes in the transgenic crops produced by different corporations
usually differ in the associated regulatory sequences such as promoter,
enhancer, terminator and intron. They also differ in codons specifying the
amino acid sequence of the final protein, having been altered in different ways
by each corporation to enhance production. The documents show that the two main
commercial transgenic maize lines differ in production of the protein by about
ten fold. Certainly the mutations are influenced by gene activity in two ways,
one way is the influence of low level toxin production which allows for greater
insect survival. The USDA documents show that there are three separate and
distinct gene insertions for Cry1Ab maize and two insertions for Bt Cry1Ac
cotton. Thus there is hidden diversity in the transgenic toxin genes. But Cry
toxin proteins are presumed to be identical even though their parent genes are
dissimilar, which is what Tabashnik has stated [2].
There is yet another caveat. For the most part, toxicity testing of the
Cry toxins was not done with the Cry toxin produced in the crops, but with the
protein produced in large scale bacterial cultures and purified. This was
allowed, even though the genes in the crops had greatly altered DNA sequences.
Thus, proteins toxins produced in bacteria were deemed identical to the toxin
protein produced in the crop, provided they had a similar molecular size using
gel electrophoresis, a relatively crude way of measuring molecular size, that
could easily conceal significant differences in the amino acid sequences
between the natural and synthetic gene product. This is yet another case of
assuming ‘substantial equivalence’ when the available evidence gives
no indication that the protein products of the transgenes for the Bt toxins are
identical to the original toxin isolated from the bacterium nor, for that
matter, to each other.
The structure and evolution of Bt toxins has been studied extensively.
Like all proteins, the toxin is separated into domains, the Bt toxin domains
are involved in insect membrane insertion and formation of pores (leading to
osmotic disruption of the cell) and membrane receptor recognition [12]. Insect
resistance is expected to disrupt the interaction between toxin and membrane,
but may also involve direct destruction of the toxin. The Bt toxins are highly
polymorphic in nature and such variability discourages rapid spread of
resistant insects.
In the final analysis, the widespread use of insecticide sprays in the
"refuge" set aside to minimize the impact of mutant insects will certainly
eliminate most resistant mutants even though such mutants are readily observed
in the laboratory experiments. However, the hidden polymorphism of the
commercial Bt crops may also reduce the spread of any resistant mutants that
survive chemical pesticides. The polymorphism of commercial Bt crops has not
received the careful scrutiny by regulators and the academic community that it
deserves.
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