Appeal No. 2001-1148 Page 6
Application No. 09/114,552
example, the ob gene (col. 10, line 30), and which are differentially expressed in
obese versus lean mice (col. 10, lines 33-41).
Accordingly, to meet the initial burden of establishing a prima facie case of
obviousness, it is incumbent on the examiner to explain how one of ordinary skill in
the art would be led to modify Tartaglia so as to produce a mouse primary
adipocyte containing a chromosome on which resides a transgene comprising a
sequence encoding a reporter.
Examiner relies on Kress and Sista for teaching the use of reporter genes.
Regarding Kress, examiner (Examiner’s Answer, p. 5) states that it
“teaches the use of promoter3/reporter4 constructs to study promoter function in
transgenic mice and transfected cells.” However, Kress does not make a knock-in
cell via homologous recombination of a native allele with a transgene containing the
reporter gene. In fact, examiner (Examiner’s Answer, p. 6) concedes that “Kress
does not teach the targeted integration of the promoter/…transgene into the …
chromosomal locus, rather chromosomal integration was random.” The result of
modifying Tartaglia in view of Kress is a reporter-containing construct that randomly
resides on the chromosome; this is in contradistinction to the specific insertion of
the reporter sequence resulting from the homologous recombination described in
3 Examiner (Examiner’s Answer, p. 5) interprets the phrase “expression regulatory sequence,” set
forth in the claims, as encompassing promoters. Based on that interpretation, the promoter
discussed in Kress is similar to that element of the claims which requires “the expression of the
reporter [to be] under the control of native gene expression regulatory sequences of the native ob
allele.”
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