Appeal No. 2002-1367 Page 11
Application No. 08/981,964
been motivated to replace the lanosterol 14-α-demethylase gene used by Kirsch
with the ACoAT gene disclosed by Hiser or Dequin. The question of motivation,
in turn, depends on whether a person of ordinary skill in the art would have
expected that the ergosterol-induced inhibition of ACoAT observed by Servouse
was a result of decreased transcription, or instead was a result of regulation at
the level of protein translation or enzyme activity.
This last possibility can be discarded quickly. Servouse discloses that
ACoAT “[e]nzyme depression is very likely due to reduced enzyme synthesis,
since we and Trocha and Sprinson have been unable to detect feedback
inhibition by ergosterol in vitro.” Page 546. Thus, those of skill in the art would
not have expected ergosterol to act directly on the ACoAT enzyme itself.
That leaves two possibilities: either ergosterol decreases ACoAT levels by
inhibiting transcription, or it decreases ACoAT levels by inhibiting translation.
What evidence of record favors each mechanism?
Appellants have provided evidence that another gene in the yeast sterol
synthesis pathway is regulated at the translational level. Specifically, Dimster-
Denk shows that mevalonate inhibits expression of the enzyme HMG-CoA
reductase in yeast, and that the regulation is carried out at the level of
translation. See the abstract. Appellants argue that Dimster-Denk “clearly
contradicts the Examiner’s assertion that a reduction in enzyme synthesis would
be reasonably expected to arise by regulation of gene transcription.” Appeal
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