GENTECH archive


Re: reply to Rick Roush on Bt resistance, archive 1150

Herve wrote,
>1) one argument more that has been said to me :
>There happen to be numerous Bt toxins and Bt genes because there are numerous
>Agrobacterium tumefaciens.

Like much of the misinformation spread to people on this list, this is
COMPLETELY WRONG. There is no relationship between these very different two
species of bacteria, Bacillus thurigiensis and Agrobacterium tumefaciens.

>.... a wide spectrum of these toxins are used while for GMO,
>if generlaized, only one toxin would be used. So one cannot compare the
>appearance of resistance in the case of multi toxins (i've been said 140)
>qith the case of only one.

Wrong again. Only three strains of Bt have had any widespread commercial
use, kurstaki (the overwhelming majority of use), tenebrionis (solely for
control of Colorado potato beetle), and most recently, aizawai (essentially
just for diamondback moth populations resistant to kurstaki).  In each
case, the overwhelming share of the mortality comes from just one toxin (or
closely related set of toxins), Cry 1A for kurstaki, Cry 3A for
tenebrionis, and Cry 1C for aizawai, which is why these toxins have been
the focus of transgenic crops.  For example, resistance to kurstaki in
diamondback moth has been shown to be due to a single gene conferring
resistance to Cry 1A and relatives.  In no way have 140 toxins been used to

In CONTRAST to Bt sprays, which have effectively developed only a few
toxins, transgenic crops are looking to develp a WIDER range of Bt
proteins, including  Cry 2 (already in cotton trials in the field) and Cry
9C (already in maize in field trials). Herve, diversity is being led by the
developers of transgenics, NOT those who use sprays!

For references, start with Tabashnik et al 1998 Philosophical Transactions
of the Royal Society, 353: 1751;  and Hofte and Whitely 1989, Microbiol
Review 53: 242.

Far more relevant as a cause of lack of resistance is that Bt is used so
little, the best proof of which is widespread resistance in the one case in
which Bt is used much at all (for diamondback moth).

>2) Second argument :
>you say :
>>I argued that EVEN IF Bt cotton lasted for only 4 years, it would help many
>You seem not to count the fact that those who use Bt as their ONLY pesticide
>would loose everything. Is it politically right not to take the freedom
>of some personns into account ?

I would be more worried about this if transgenic crops were any serious
threat to those who use Bt sprays.  Let's get specific; just what pests
targetted by transgenic crops get any Bt sprays now?  Give me some
examples. For example, cotton bollworms don't eat apple crops that might be
treated with Bt sprays. There are a few possible cases, like potatoes and
Colorado potato beetles, and I'll be happy to explain to anyone who wants
the details  why these do not worry me.   Most Bt used now is applied
against diamondback moth on cabbages and the like, and budworms in Canadian
forestry, nethier of which are targetted by Bt transgenic crops in

Herve, the problem is just the opposite. Is it politically right for a
small minority of people, who aren't likely to be adversely affected anyway
and are acting largely on misinformation and ignorance about the biology of
the pests, to prevent a much larger group of farm workers from benefitting
from Bt crops?

>3) Last, an old arguemnt : even if we can find other peesticide (remains to
>be proved), wouldn't they be more toxic ? Then you will "help many people"
>in a short term, but injury them after ...

Herve, I don't understand your argument.
>4) you said :
>>there is no DNA or protein in cotton seed oil once
>>it has been processed for food
>You mean there are only traces. This said, I trust that there are much
>less risks in the alimentary than in the environment.

Herve, so far as I am aware, there is NO detectable DNA or protein left in
cotton seed oil, and by that I mean that there are no traces even through
the most sophisticated techniques (if you can't detect anything, how can
there be traces?).  Do you have evidence (like a publication, not some
hearsay spread on the net) to the contrary?

>5) you said :
>>resistance in the pests
>Please, what is the gene of resistance to pests ? I only know genes of
>production of insecticides.

In the case of diamondback moth, a major gene  seems to be one controlling
decreased sensitivity of the pest at the site in the gut that binds the Cry
protein. See the Tabashnik paper as cited above.
>6)  you said :
>>pesticide sprays, which can also persist in the soil and are
>>much less selective
>Sorry, I cannot understand the difference. I thought selectiveness was
>the ability to kill a selective weed or pest. Why the spray should be less
>selective ? Moreover, I thought that the most dangerous pesticides were
>more selective. WHat's my mistake ?

By "selective", I mean pesticides that kill the pest and nothing else.
Chemical sprays tend to kill more than the pest, due to their lack of
selectivity.  Is this clearer?