Interference 103,781
plants because it didn’t have the right codon frequency for
a plant gene to be expressed well, because I knew any gene
that was 70 to 80 percent AT-rich would necessarily have to
have a different codon usage than a plant gene which are 50
to - 45 to 55 percent GC-rich depending on, you know, which
plant you’re looking at.
It also occurred to me that some mechanism that did not
allow very good initiation of transcription might occur such
that you weren’t getting very much transcription at all
starting at the very 5 prime end. The whole promoter might
not work particularly well.
But on the whole, I tended to think that those were not
because of the promoter we had put in front of the Bt gene,
the mannopine promoter, but that there might be some
regulatory sequences within the 5 prime end of the Bt gene,
you know, or anywhere in the Bt gene for that matter such
that a, you know, some kind of transcription factor might
come in and bind these sequences and block transcription.
And I thought that was another possibility.
I - there may have been other possibilities. I did
think splicing was a possibility.
We talked about splicing at the group, and I’m not sure
I’m the one that first thought of it. I seem to recall
other people mentioned splicing to me. And then I say said,
I think that could be another reason why we have a truncated
RNA.
And then because splicing also involves some kind
of site specific cleaving of the RNA, and then you require
another mechanism to past the two pieces back together
again once you’ve cleaved out a region. You know, it
could be that the cutting part worked well, and then the
pasting together part didn’t work too well, and so that
would lead to RNA turnover as well.
Q. Have you finished your answer?
A. Those are the - those are the main mechanisms that
I can recall at this time.
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