Appeal No. 1999-1157
Application No. 08/482,321
1988) where the court found that the prior art was required only to
“reveal reasonable expectation of success in producing the claimed
invention”. One would have expected a stronger attenuator deleted
tryptophan promoter-operator system because intracellular tryptophan
regulates repressor affinity for operator as well as trp E and trp D by
feedback inhibition-thus two points of regulation exist that do not exist
in an analogous way in the lac-operon system.
We are not persuaded by the examiner’s arguments. With regard to the
examiner’s argument concerning two points of regulation, appellants’ specification
(page 4) explains that “[i]n wild-type E. coli, the tryptophan operon is under at least
three distinct forms of control.” Two of which are regulated by tryptophan. With
regard to the point of control not regulated by tryptophan, the specification (page 4)
explains that this “control is effected by a process known as attenuation under the
control of the ‘attenuator region’ of the gene, a region within the trp leader
sequence.” Appellants’ claimed invention specifically excludes this “attenuator
region,” see claim 1 “said sequence comprising neither any trp attenuation
capability nor nucleotides coding for the trp E ribosome binding site.” With regard
to the two points of control regulated by tryptophan, the specification discloses
(page 4) that one is “by a process of feedback inhibition, tryptophan binds to a
complex of the trp E and trp D enzymes, prohibiting their participation in the
pathway [of tryptophan] synthesis.” Therefore, since appellants’ construct is not
involved in tryptophan synthesis this point of regulation does not appear to be a
relevant point of control for the instant invention.
With regard to the second point of control regulated by tryptophan,
appellants’ specification (page 4) explains “tryptophan acts as a corepressor and
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