On 17 Aug 2003 12:53:23 GMT, Brian Sandle
posted:

Mooshie peas wrote:
On Fri, 8 Aug 2003 17:15:49 +0100, Oz
posted:

Torsten Brinch writes
On Fri, 08 Aug 2003 04:20:48 GMT, "Moosh:}"
wrote:

On Thu, 07 Aug 2003 07:20:22 -0700, Walter Epp
posted:
[Quoting Independent on Sunday (London) March 30, 2003:]
.. Environmentalists say that resistance develops all the faster
because the insects are constantly exposed to it in the plants, rather
than being subject to occasional spraying.

Occasional spraying will result in many occasions where dose is
sublethal. Ideal circumstances for resistance development.

Only if too little is applied.

And when too little is present. And this will be after EVERY
application, as an application necessarily wanes.

So with organic Bt a heavy dose is applied
when needed.

That would be constantly during a pest presence? You're dreaming.
Only BT expression can do this.

It degrades quite quickly so new generations of insects are
not exposed to it.

How long does it take to become a sublethal presence? How long does a
sub-lethal level occur with intermittent application. How do you
ensure that every pest that takes a bite from the crop gets a lethal
dose. I put it to you that that's impossible without the even
expression of the 'cide within the crop, continuously.

With GM Bt crops the dose much more gradually decreasses as the crop
ripens.

But the pests are not feeding then?

However, reminding ourselves of the perils of assumption-based
reasoning, let us hear what the experienced farmers over at
sci.agriculture has to say about that.

There are two arguments:

1) Apply full dose and kill 99.999% except the 0.001% that have a
resistance gene and next season you will have a 100% resistant
population. If (as is common) you have a pest with a very high
reproductive rate then you are stuffed in a year or two.

This is what happened for dimfop resistant blackgrass.
This might be typical of single gene resistance (not tolerance).

This will happen whether or not the gene is less efficient than the
'natural' gene.

2) Apply a reduced rate, kill 99% of the pest, leave 1% of which 1:1000
have a resistance gene. Hope the resistance gives less efficient pest,
outbred by 'natural' genes, leaving a final pest population still with
about 0.001% resistance. So no change.

Most field weeds are more tolerant of pesticides than their wild
relatives, but often not by much.

Pesticides acting on single genes are MUCH more likely to become
completely useless due to single point mutation.

Pesticides with multiple-point action are pretty unlikely to develop
resistance.

Obviously simultaneously using several pesticides with different action
mimics multiple-point resistance.

If a pesticide targets a key site, that is hard for the pest to alter
because it is critical (perhaps used in many subsystems or is very
basic), then tolerance rather than resistance seems to be the normal
mode of action (eg hormone weedkillers, IPU). I haven't seen it stated,
but I suspect the progeny are less competitive.

Certainly resistant blackgrass seems to be highly susceptible to mildew,
for example.

Bottom line though is that BT expressed is no more likely fo cause
resistance development problems than intemittent application of BT.

No it is, because it always there selecting a bit.

It can only select when pests are feeding, and when some pests are
surviving it. Intermittent allows this after every application.
Expression ensures a lethal dose at every bite (theoretically)

Why do you think the NZ
Royal Commission recommended education about refuges before releasing GM
crops?

The NZ RC has a bad taste in it's mouth after that lady professor lied
to them with phony evidence.

Aren't the refuges for pest predators? Why would you want refuges for
the pests?