Interference 103,781
(AX 101B), had a poly-A tail (AR 6040, p. 1426, l. 9-14), and
that because the RNA had a poly-A tail, they knew that there
were poly-A sites in the middle of the Bt gene that had to be
eliminated by removal or modification to enhance expression of
the Bt toxin gene in plants (AR 6040, p. 1428, l. 12-15). Dr.
Adang’s testimony suggests that all their knowledge about poly-A
tails and poly-A sites, their concept of removing or modifying
poly-A sites from Bt toxin genes, and the basis therefor, were
written down in Dr. Murray’s laboratory notebook (AX 101B) and
Dr. Adang’s draft abstract for the UCLA symposium talk (AX 106E)
(AR 6040, p. 1428, l. 25, to p. 1430, l. 2). To the contrary,
we find no evidence in either Dr. Murray’s laboratory notebook
(AX 101B) or Dr. Adang’s draft abstract for the UCLA symposium
talk (AX 106E) that either Dr. Murray or Dr. Adang knew that the
chopped-up RNA found via Dr. Murray’s Bt Northerns had poly-A
tails or that poly-A sites in Bt toxin genes were causing
premature termination of transcription and thus unacceptably low
expression of Bt toxin genes in plants. Rather, the closest
concept to the invention of Count 2 that we can find expressed
in Dr. Murray’s lab notebook (AX 101B) and Dr. Adang’s draft
abstract for his UCLA talk (AX 106E) is their common recognition
that, at least for tobacco plants, “Bt may have some kind of
premature termination signal . . . where the transcription was
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