Appeal No. 1995-2789
Application No. 07/788,114
other homoserine dehydrogenase mutants which are insensitive to feedback
inhibition by threonine.” However, as the examiner explains (id.), Reinsheid
“does not teach a mutant homoserine dehydrogenase which has a single base
deletion in codon 429.”
The examiner relies on Winnacker to make up for this deficiency.
According to the examiner (Answer, page 9) Winnacker “teaches a general
method of producing deletion or localized point mutations within a gene.” Based
on the teachings of Reinscheid and Winnacker the examiner concludes (Answer,
page 9), “one of ordinary skill in the art would have been motivated to have
mutagenized [using the techniques of Winnacker] the suggested carboxy
terminus of the homoserine dehydrogenase gene for its known and expected
benefit.”
In response appellants argue (Brief, pages 23 and 24) that the prior art
relied upon by the examiner fails to provide the motivation or suggestion “to
make the proposed modifications needed to arrive at the claimed invention.” At
page 24 of the Brief, appellants emphasize that the references fail to:
suggest or imply a single base deletion in the nucleotide sequence
encoding amino acid 429 of the hom gene … as specified in [c]laim
6, a truncated homoserine dehydrogenase protein as specified in
[c]laim 10, a homoserine dehydrogenase protein truncated after
amino acid 438 as specified in [c]laim 11, or a homoserine
dehydrogenase having the specific nucleotide or amino acid
sequence as specified in [c]laims 12 and 13.
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