DETAILED ACTION
Notice of Pre-AIA or AIA Status
The present application, filed on or after March 16, 2013, is being examined under the first inventor to file provisions of the AIA .
Election/Restrictions
Applicant elected Group III, claims 2 and 9-16, without traverse.
Claim Status
Claims 1-26 are pending; Claims 2 and 9-16 are examined on the merits; Claims 1, 3-8, and 17-26 are withdrawn from consideration pursuant to the restriction requirement.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
Claims 2 and 9-16 are rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 2 recites Nic1 and Nic2 ERF genes comprising specified nucleotide or amino acid sequences or a “functional variant or orthologue thereof”. Although the specification defines a “functional variant” as variability occurring “without significant loss of activity”, it is unclear whether the retained activity refers to general ERF activity or the specific nicotine-biosynthesis activity of the disclosed Nic1/Nic2 ERFs. The disclosed Nic1 ERFs are associated with the Nic1 locus and nicotine phenotype, whereas structurally similar ERFs outside the locus may not participate in nicotine biosynthesis. The specification also does not provide an objective standard for determining what degree of loss constitutes a “significant loss”.
The specification further defines an “orthologue” may share at least 70% sequence identity and often share the same or similar functions. However, sequence similarity or ortholog does not provide a definite boundary.
Accordingly, the scope of “functional variant or orthologue thereof” is unclear.
Dependent claims 9-16 are included in this rejection because they do not include additional limitations to resolve the ambiguity.
Claim Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Written Descriptions
Claims 2 and 9-16 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
The Federal Circuit has clarified the application of the written description requirement. The court stated that a written description of an invention "requires a precise definition, such as by structure, formula, [or] chemical name, of the claimed subject matter sufficient to distinguish it from other materials". University of California v. Eli Lilly and Co., 119 F.3d 1559, 1568; 43 USPQ2d 1398, 1406 (Fed. Cir. 1997). The court also concluded that "naming a type of material generally known to exist, in the absence of knowledge as to what that material consists of, is not description of that material". Id. Further, the court held that to adequately describe a claimed genus, Patent Owner must describe a representative number of the species of the claimed genus, and that one of skill in the art should be able to "visualize or recognize the identity of the members of the genus". Id.
The claims are rejected for lacking adequate written description support regarding the broad scope of the following.
Claim 2 recites a modified plant, plant part, plant propagation material, or modified cell culture having decreased alkaloid content, wherein the modification decreases the activity or expression of both a Nic1 ERF gene and a Nic2 ERF gene. The Nic1 and Nic2 ERF genes are defined not only by specifically recited nucleotide and amino acid sequences, but also by a “functional variant or orthologue”. Claim 9 similarly encompasses a Nic1 ERF corresponding to SEQ ID NO: 8 and a Nic2 ERF corresponding to SEQ ID NO: 72, or functional variants or orthologues hereof. Claims 10-16 depend directly or indirectly from claim 2 and therefore remain this breadth.
The specification defines a “functional variant” as variability in genomic sequences occurring “without significant loss of activity” in gene and/or protein function, and expressly states that sequences having a degree of sequence identity or homology to the disclosed sequences may constitute functional variants (pa0408). The specification further states that functional variants may differ from the disclosed sequence by amino-acid substitutions and include variants differing by one through ten amino acids (pa0408-0410).
The claimed “orthologue” genus is substantially broader. The specification defined an orthologue as a gene derived from a common ancestral gene and found in a different species as a result of speciation, and states that orthologues may share only 70%, 75%, 80%, 85%, 90%, 91%, 92%, 93%, 94%, 95%, 96%, 97%, 98%, 99% or greater sequence identity at the nucleotide sequence and or amino acid sequence level (pa0411). The specification likewise describes Nic1-related polynucleotides having as little as 70% identity to the disclosed sequence (pa0396). For Nic2 ERFs, the specification expressly contemplates mutations in sequences encoding the disclosed Nic2 proteins or proteins having at least 70% identity thereto (pa0277).
Thus, the claimed genus is not limited to the specially identified N. tabacum ERFs. It extends to structurally divergent ERF sequences, including ERFs from species other than N. tabacum, provided they satisfy the functional characterization recited in the claims.
The specification provides meaningful experimental support for particular N. tabacum Nic1 ERFs, especially ERF199. Example 12 reports that overexpression of Nitab4.5_0003090g0030.1/ERF199 and two additional Nic1 ERFs significantly increased alkaloid content, with ERF199 overexpression restoring alkaloid levels to levels comparable with HI plants (pa0650-0651). Example 13 further reports that a homozygous Q25* premature-stop mutation in ERF199 resulted in plants containing approximately one-third of the alkaloid content of wild-type controls (pa0652-0655). The specification additionally states that an ERF199 knockout in an HI/nic2 background produced alkaloid content below that of LA Burley 21, and that combining the nic2 mutation with the ERF199 mutation produced a greater-than-additive reduction in alkaloids (pa0608-0611).
These disclosures reasonably show possession of specific tobacco ERF embodiments. They do not, however, provide representative examples commensurate with the substantially broader genus of functional variants and orthologues encompassed by the claims. In particular, the specification does not identify representative functional variants spanning the claimed sequence divergence, representative orthologues from different plant species, or representative combinations of such Nic1 and Nic2 orthologous that have been demonstrated to retain the claimed alkaloid-regulatory function.
The specification states generally that homologous sequences should retain functional activity and generally retain the same active sites, domains, or motifs (pa0560-0562). However, the specification does not identify a structural feature, set of residues, domain architecture or other structure/function correlation that distinguishes members that regulate alkaloid biosynthesis in the claimed manner from ERF-family members that do not.
The absence of such a correlation is particularly significant because the available ERF evidence demonstrates functional specialization within the ERF family rather than uniform function based merely on ERF-family membership or sequence relatedness. Shoji (Tsubasa Shoji et. al., Phytochemistry (2015) 113, pp41–49), for example, report that ERF189 and ERF199 constitute a homologous pair whose expression patterns imply their specific involvement in nicotine-pathway regulation and the exclusion of other ERF-family members from that function (p46, left column, pa2). Shoji explains that a NIC2-locus ERF, and the closely related ERF199 homolog exhibit strong regulatory activity in nicotine biosynthesis relative to other related ERF-family members. (p41-42, “Introduction”).
Shoji (Tsubasa Shoji et. al., The Plant Journal (2011) 67, pp949–959) likewise teaches that ERF189 was the most effective NIC2-locus EFR in various functional assays, and further identify sequence-specific DNA-binding characteristics of ERF189 (p956-957, “Evolution of duplicated QPT genes in tobacco”). These teachings reinforce that biological activity within the ERF family depends upon particular regulatory and structural characteristics and cannot reasonably be inferred merely from membership in a broad ERF sequence genus.
Accordingly, although the specification demonstrates possession of particular disclosed N. tabacum ERFs, including ERF199 and disclosed Nic1/Nic2 combinations, the disclosure does not provide a representative number of species or common structural features sufficient to demonstrate possession of the entire genus of functional variants and orthologues, including sequence-divergent and cross-species members encompassed by claims 2 and 9-16.
Scope of Enablement
Claims 2 and 9-16 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specifications, while being enabling for the specific disclosed N. tabacum ERF189 and ERF199 sequences, and conventional methods for decreasing the activity or expression of those disclosed ERFs to reduce alkaloid content, does not reasonably enable the full scope of ERF189/ERF199 functional variants and orthologues in claims. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
An “analysis of whether a particular claim is supported by the disclosure in an application requires a determination of whether that disclosure, when filed, contained sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention.” MPEP 2164.01. “A conclusion of lack of enablement means that. . . the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention [i.e. commensurate scope] without undue experimentation.” In re Wright, 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993); MPEP 2164.01.
In In re Wands, 858 F.2d 731,8 USPQ2d 1400 (Fed. Cir. 1988), several factors implicated in determination of whether a disclosure satisfies the enablement requirement and whether any necessary experimentation is “undue” are identified. These factors include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. In re Wands, 858 F.2d 731,737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). No single factor is independently determinative of enablement; rather “[i]t is improper to conclude that a disclosure is not enabling based on an analysis of only one of the above factors while ignoring one or more of the others.” MPEP 2164.01. Likewise, all factors may not be relevant to the enablement analysis of any individual claim.
Claim 2 encompasses specifically identified Nic1 and Nic2 ERFs as well as functional variants and orthologues thereof, and claim 9 similarly encompasses functional variants and orthologues of the Nic1 ERF corresponding to SEQ ID NO: 8 and the Nic2 ERF corresponding to SEQ ID NO: 72. Claims 10-16 inherit this scope.
Under the specification’s definitions, the claimed scope extends substantially beyond the specifically characterized ERFs. A functional variant includes sequence variation that retains relevant activity, while an orthologues may be a gene from another species having as little as 70% nucleotide or amino-acid sequence identity to the disclosed sequence (pa0408-0411). Thus, practicing the full scope requires more than modifying the specifically disclosed N. tabacum ERF199 and ERF189 sequences. The specification provides substantial guidance concerning how to decreased expression or activity of an already-selected ERF gene. It states that Nic1 and Nic2 ERF activity or expression may be inhibited using gene editing, targeted mutagenesis, RNA interference, antisense suppression, or sense co-suppression (pa0366-0368). It further provides CRSISPR/Case9 procedures and gene-editing vector construction and target oligonucleotides (pa0396). Therefore, the enablement deficiency is not the mechanical ability to mutate or suppress a known ERF gene. Rather, the deficiency is determining which members of the broad functional-variant and orthologue genus actually possess the Nic1 and Nic2 activity required to produce the claimed decrease in alkaloid content.
The specification demonstrates operability of particular tobacco ERFs. for example, ERF199 overexpression increases alkaloid production, whereas the Q25* ERF199 mutation reduced alkaloid content to approximately one-third levels (pa0650-0655). The specification also demonstrates a strong reduction when the ERF199 mutation is combined with the nic2 background (pa0608-0611).
However, the specification does not establish a predictable relationship between the degree of sequence identify recited for the broader genus and the claimed alkaloid-regulatory activity. Although the specification generally indicates that homologous sequences should retain functional activity and domains or motifs, it does not identify which structural characteristic must be retained to preserve regulation of the nicotine/alkaloid pathway (pa0560-0562). The evidence in the art further indicates that ERF function is not uniform even among related ERFs. Shoji (2015) reports that only a subset of NIC2-locus ERFs and homologs, including ERF189 and ERF199, were particularly effective in nicotine-pathway regulation (pp41-43, “Introduction”). More specifically, ERF189 and 199 exhibited expression patterns implying their specific involvement in nicotine biosynthesis and the exclusion of other ERF family members from that function (Abstraction). Shoji (2011) reports that ERF 189 is the most effective among the NIC2-locus ERFs in regulating nicotine biosynthesis and shows that particular residues and DNA-binding characteristics distinguish ERF189/claide2-1 ERFs from other ERFs (p956, “Binding site preference of ERF189”). Shoji (2011) further demonstrates that ERF189 positively regulates QPT2 but not QPT1: ERF189 overexpression increased QPT2 expression two-to three-fold, while dominant repression reduced QPT2 approximately 15-25% of control levels (p 952, Fig. 2). This functional specificity indicates that ERF-family membership or general sequence similarity alone does not predict the claimed biological activity.
Accordingly, for a candidate functional variant or orthologue falling within the board genus, a skilled artisan would have to at least, identify a candidate sequence; determine whether the candidate retains the relevant nicotine/alkaloid regulatory function; determine whether it acts as the claimed Nic1 or Nic2 ERF in the selected plant species; reduce or eliminate its activity/expression; generate the modified plant or cell; and assay whether the modification produces the claimed decrease in alkaloid content.
The specification provides assays by which some of these steps can be performed (pa0328-0335). These assays make screening technically possible, but they do not provide the missing predictive guidance identifying which members of the broad calmed sequence genus will have the required pathway-specific function.
The breadth of the claims is substantial because claims 2 and 9 are not restricted to the experimentally characterized tobacco sequences and encompass sequence-divergent variants and orthologues from different species, including orthologues having as little as 70% sequence identity.
The mature of the invention and predictability of the art weigh against enablement of the full genus because the claimed result depends on a transcription factor retaining a particular regulatory role in the alkaloid pathway. The evidence shows functional differentiation even among related ERFs; only selected family members such as ERF189 and ERF199 have the particularly strong or specific nicotine-regulatory function.
The amount of guidance is substantial regarding techniques for suppressing a selected gene, but limited regarding how to identify, form sequence structure, which functional variants and cross-species orthologues possess the required alkaloid-regulatory activity. The specification provides no sufficient structure/function rule that substitutes for functional testing.
The working examples are concentrated on specific N. tabacum ERFs, particularly ERF199, rather than representative variants spanning the claimed degree of sequence divergence or representative orthologues from different species.
The quantity of experimentation therefore becomes substantial over the full scope because candidate members must be selected and functionally screed to determine whether they regulate the alkaloid pathways as required. Although the individual assays and gene-editing techniques are known, repeated screening across the structurally and taxonomically broad claimed genus would be required in the absence of predictive structural guidance.
Accordingly, although the specification enables particular disclosed N. tabacum ERFs and conventional methods for decreasing their activity or expression. It does not reasonably enable the full scope of the functional variants and orthologues encompassed by claims 2 and 9-16 without undue experimentation.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
Claims 2 and 9-16 are rejected under 35 U.S.C. §103 as being unpatentable over Shoji (Tsubasa Shoji et. al., The Plant Cell (2010) Vol. 22: 3390–3409), in view of Shoji (2015).
For clarity, Shoji uses NIC1 and NIC2 to refer to two genetic loci regulating nicotine biosynthesis, while nic1 and nic2 refer to mutant alleles or mutant backgrounds at those respective loci (Shoji 2010, p3391). Shoji further identifies ERF 199 and ERF 189 as closely related ERF transcription factors associated with NIC1- and NIC-2regulatory systems, respectively (Shoji 2010, pp3392-3393, Fig. 1). As discussed below, sequence comparison further establishes that ERF199 corresponds to the claimed Nic1 ERF and ERF189 corresponds to the claimed Nic2 ERF.
Claim 2 recites a modified plant, part thereof or a plant propagation material obtainable therefrom, or a modified cell culture which has decreased alkaloid content in comparison to a control plant or control cell culture, wherein the modification decreases the activity or expression of a Nic1 ERF gene and a Nic2 ERF gene, and wherein the modification of the Nic1 ERF gene is not present in LA Burley 21.
Shoji (2010) identifies ERF189 and ERF199 as closely related clade 2-1 ERF transcription factors, groups them in an ERF189/ERF199 cluster, and teaches that their AP2/ERF DNA-binding domains are identical in amino-acid sequence (p3392, Fig. 1).
Shoji (2010) additionally teaches that suppression of NIC2-locus ERFs decreases nicotine biosynthesis and alkaloid content. ERF189 RNAi reduced ERF189 and related clade-2 ERF expression and resulted in decreased nicotine-biosynthetic gene expression and decreased tobacco alkaloid levels (p3395-3397; Fig. 5). The ERF198 sequence deposited by Shoji (2010) as GenBank Accession NO. AB827951.1 encodes an amino acid sequence that is 100% identical to SEQ ID NO: 72 of the instant application. Shoji (2015) further identifies ERF199 and provides ERF199-specific primers designed from the corresponding tobacco genomic sequence. Sequence analysis using these primers identifies GenBank Accession No. LC903786.1, whose encoded ERF199 protein differs by only one amino acid from, and is 99.58% identical to , SEQ ID NO: 8. Thus, the ERF198 and ERF199 proteins taught by the /Shoji references correspond to the claimed Nic2 and Nic1 ERFs, respectively (sequence information, alignment see below).
Shoji (2015) further identifies ERF189 and ERF199 as a homologous regulatory pair particularly involved in nicotine-biosynthetic pathway regulation, and explains that the two proteins possess nearly identical DNA-binding domains and would be expected to exhibit substantially the same DNA-binding specificity (p46, “3.2. Nicotine (1) pathway regulation by ERF189 and ERF199”).
It therefore would have been obvious to one of ordinary skill in the art seeking to decrease tobacco alkaloid content to decrease the activity or expression of both ERF199 and ERF189. Shoji (2010) establishes that decreasing nicotine-regulatory ERF activity reduced nicotine-biosynthetic gene expression and alkaloid levels and that NIC1 and NIC2 exhibit synergistic effects; shoji (2010) confirms the positive regulatory role of ERF189; and Shoji (2015) identifies EFR189 and ERF199 as the homologous pair particularly implicated in nicotine-pathway regulation. One of ordinary skill therefore would have had a reasonable expectation that decreasing both positive regulatory ERFs would decrease nicotine biosynthesis and alkaloid content.
With respect to the limitation that the modification of the Nic1 ERF gene is not present in LA Burley 21, Shoji (2010) teaches that the low-nicotine Burley 21 line carrying the nic1 and nic2 regulatory mutations and explains that the two mutations reduce nicotine levels and exhibit synergistic effects (p3391, right column, pa2). Accordingly, it would have been obvious to introduce an additional engineered modification affecting ERF activity that is not the pre-existing Nic1 modification of LA Burley 21.
Accordingly, claim 2 would have been obvious over Shoji (2010) and Shoji (2015).
Claim 9 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein: the Nic1 ERF gene encodes a polypeptide which comprises an amino acid sequence as set out in SEQ ID No. 8 or a functional variant or orthologue thereof; and the Nic2 ERF gene encodes a polypeptide which comprises an amino acid sequence as set out in SEQ ID No. 72 or a functional variant or orthologue thereof. Claim 10 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the modification of the Nic1 ERF gene and the Nic2 ERF gene in combination is not present in LA Burley 21.
For the same reason set forth above with respect to claim 2, Claim 9 and 10 would have been obvious over Shoji (2010) and Shoji (2015).
Claim 11 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the modification eliminates the Nic1 ERF gene activity and/or the Nic2 ERF gene activity.
For the same reason set forth above with respect to claim 2, Shoji (2010) teaches low-nicotine Burley 21 lines in which the nic1 and nic2 mutations at the NIC1 and NIC2 regulatory loci reduce nicotine levels, with the nic1 mutation having a stronger effect than nic2 and the two mutations exhibiting synergistic effects (p3390, right column, pa2). Shoji (2010) further teaches that the nic2 mutation comprises a deletion encompassing NIC2-locus ERF genes (p3395, left column, pa2-3), thereby eliminating activity of those ERF genes and contributing to the low-nicotine phenotype. Thus, Shoji 2010 teaches elimination of Nic2 ERF gene activity as recited in claim 11.
Claims 12 recites the plant, part thereof, plant propagation material or cell culture according to claim 11, wherein the modification:(i), (ii), (iii), (iv), (v), (vi) (vii), (viii), or (ix).
For the same reason set forth above with respect to claim 11, Shoji (2010) expressly teaches RNA interference, corresponding to alternative (viii) of claim 12 (p3395-3397, Fig.5A-B). Shoji (2010) additionally identifies an ERF104 frameshift mutation producing a truncated protein, demonstrating that loss-of function alterations in this ERF family were known (p3392, right column, pa3).
Claim 13 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the total alkaloid content of the plant or cell culture is decreased in comparison to a control plant or control cell culture. Claim 14 recites plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the total alkaloid content is decreased by at least 80% in comparison to a control plant or control cell culture. Claim 16 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the nicotine content is decreased.
For the same reason set forth above with respect to claim 2, Shoji (2010) expressly determines levels of the tobacco alkaloids nicotine, nornicotine, anabasine, and anatabine and teaches that suppression/dominant repression of the ERFs decreases these alkaloids. Shoji (2010) reports approximately 87-98% reductions in tobacco alkaloids levels in ERF dominant-repressor lines, thereby teaching a decrease of at least 80% (p3397, Fig. 5E).
Claim 15 recites the plant, part thereof, plant propagation material or cell culture according to claim 2, wherein the plant or plant cell is from the Nicotiana genus.
Shoji (2010) performs the relevant ERF suppression studies in tobacco, Nicotiana tabacum (Abstract).
Accordingly, claims 11-16 would have been obvious over Shoji (2010) and Shoji (2015).
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Double Patenting
The nonstatutory double patenting rejection is based on a judicially created doctrine grounded in public policy (a policy reflected in the statute) so as to prevent the unjustified or improper timewise extension of the “right to exclude” granted by a patent and to prevent possible harassment by multiple assignees. A nonstatutory double patenting rejection is appropriate where the conflicting claims are not identical, but at least one examined application claim is not patentably distinct from the reference claim(s) because the examined application claim is either anticipated by, or would have been obvious over, the reference claim(s). See, e.g., In re Berg, 140 F.3d 1428, 46 USPQ2d 1226 (Fed. Cir. 1998); In re Goodman, 11 F.3d 1046, 29 USPQ2d 2010 (Fed. Cir. 1993); In re Longi, 759 F.2d 887, 225 USPQ 645 (Fed. Cir. 1985); In re Van Ornum, 686 F.2d 937, 214 USPQ 761 (CCPA 1982); In re Vogel, 422 F.2d 438, 164 USPQ 619 (CCPA 1970); In re Thorington, 418 F.2d 528, 163 USPQ 644 (CCPA 1969).
A timely filed terminal disclaimer in compliance with 37 CFR 1.321(c) or 1.321(d) may be used to overcome an actual or provisional rejection based on nonstatutory double patenting provided the reference application or patent either is shown to be commonly owned with the examined application, or claims an invention made as a result of activities undertaken within the scope of a joint research agreement. See MPEP § 717.02 for applications subject to examination under the first inventor to file provisions of the AIA as explained in MPEP § 2159. See MPEP § 2146 et seq. for applications not subject to examination under the first inventor to file provisions of the AIA . A terminal disclaimer must be signed in compliance with 37 CFR 1.321(b).
The filing of a terminal disclaimer by itself is not a complete reply to a nonstatutory double patenting (NSDP) rejection. A complete reply requires that the terminal disclaimer be accompanied by a reply requesting reconsideration of the prior Office action. Even where the NSDP rejection is provisional the reply must be complete. See MPEP § 804, subsection I.B.1. For a reply to a non-final Office action, see 37 CFR 1.111(a). For a reply to final Office action, see 37 CFR 1.113(c). A request for reconsideration while not provided for in 37 CFR 1.113(c) may be filed after final for consideration. See MPEP §§ 706.07(e) and 714.13.
The USPTO Internet website contains terminal disclaimer forms which may be used. Please visit www.uspto.gov/patent/patents-forms. The actual filing date of the application in which the form is filed determines what form (e.g., PTO/SB/25, PTO/SB/26, PTO/AIA /25, or PTO/AIA /26) should be used. A web-based eTerminal Disclaimer may be filled out completely online using web-screens. An eTerminal Disclaimer that meets all requirements is auto-processed and approved immediately upon submission. For more information about eTerminal Disclaimers, refer to www.uspto.gov/patents/apply/applying-online/eterminal-disclaimer.
Claims 2 and 9-16 rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1-8, and 12-17 of U.S. Patent No. 12139718. Although the claims at issue are not identical, they are not patentably distinct from each other because instant claim 2 recites a modified plant, plant part, plant propagation material, or modified cell culture having decreased alkaloid content, wherein the modification decreases the activity or expression of a Nic1 ERF gen and a Nic2 ERF gene. The patent claims methods of decreasing alkaloid content in tobacco by eliminating activity of the same Nic 1 and Nic2 ERFs recited in the present claims, including the Nic1 ERF encoding SEQ ID NO: 8 and, in claims 5, 6, 12, and 13, additionally eliminating activity of a Nic2 ERF encoding SEQ ID NO: 72. Practicing the patented methods would result in tobacco plants or cells having decreased activity of the recited Nic1 and Nic2 ERFs and decreased alkaloid content. Therefore, the presently claimed products would have been an obvious result of practicing the previously patented methods.
In particular, patent claim 6 requires elimination of activity of the Nic1 ERF encoding SEQ ID NO: 8 together with the Nic2 ERF encoding SEQ ID NO: 72, corresponding to the ERF combination recited in present claim 9, and patent claims 14 and 16 additionally require at least an 80% decrease in total alkaloid content, corresponding to present claim 14. The additional limitations of present claims 10-13 and 15-16 likewise do not render the claims patentably distinct because they further define particular embodiments of the same Nic1/Nic2 ERF modifications and resulting tobacco material encompassed by the patented claims.
Accordingly, the presently claimed subject matter is an obvious variation of the subject matter claimed in U.S. Patent No. 12139718.
Conclusion
No claims are allowed.
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/YANXIN SHEN/ Examiner, Art Unit 1663
/WEIHUA FAN/ Primary Examiner, Art Unit 1663
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