Interference 103,781
to show where the transcription was terminating. Then
we could use the sequence information to site specifically
mutagenize the premature termination region of the Bt gene.
Fact 35 also cites the record at AR 6040 (1427:18-1428:17) in
further support of the quotation above taken from Dr. Murray’s
lab notebook (AB 10). AR 6040 is a record of Dr Adang’s
testimony in Delaware I (AR 6019; AR 6039, p. 1424, l. 18-19).
With reference to the entries on Dr. Murray’s lab notebook, p. 13
(AX 101B), Dr. Adang testified (AR6039-6041, pp. 1424, l. 18,
to 1430, l. 2)(emphasis added):
Q. Dr. Adang, going back to 1985, could you describe what
work you were doing at Agrigenetics at that time?
A. In the summer of 1985, we were working on the expression
of native Bt genes in tobacco plants. We had – we had put
insects on these plants and we had observed that -we saw
some kill the worms on these plants, but these Bt tobacco
plants weren’t killing the worms at a commercially-useful
level.
We also saw a mono Bt protein in these tobacco plants
was very, very low. So in the summer of ‘85 and continuing
on, we started thinking about and working on trying to
figure out what was happening in these plants, why the Bt
gene wasn’t working better. And we knew that we needed a
solution to coming [sic] up with, you know, solving this
problem of low Bt expression.
Q. And did you arrive at a solution at that time?
A. Yes, we did. In late 1985, Dr. Liz Murray and I came
up with the solution of modifying Bt genes to make them
more plant-like. And as part of these modifications, we
would also remove a poly - remove poly-A sites.
Q. Who was Dr. Murray?
-96-
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