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 .
Status of the Claims
Claims 1-20 are pending and they are examined in this office action.
Claim Objections
Claim 1 is objected to because of the following informalities: In claim 1 line 2, the claim recites the term “frequenct” which is advised to change to the right term “frequency”.
Appropriate correction is required.
Claim Rejections - 35 USC § 112 - Indefiniteness
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 1-20 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. All dependent claims are included in these rejections unless they include a limitation that overcomes the deficiencies of the parent claim.
Regarding claim 1, the claim lines 4-5 recite “the causative gene or region is located within an endogenous genomic locus”, lines 5-6 recite the “the location of the causative gene or region within the endogenous genomic locus is unknown”, lines 8-10 recite “introducing at least two different site-specific deletions at two or more native target sequences in the endogenous genomic locus in a plurality of plants of the plant line, thereby creating a plurality of targeted deletion plants”. The recitation renders claim indefinite since applicant in line 4 recites the location of the causative gene or region is known and it is within endogenous genomic locus wherein in line 5 it recites the gene or region is unknown. It is not clear what does “unknown” means since the location is known and the method line 8 further recite introducing “site-specific” deletions and creating “targeted deletions plants” which would require specific regions of the gene to be known. It is not clear how does a site-specific and targeted deletions are created without knowing the region.
Furthermore, the structure of the “region” is unknown, a region of a gene would comprise any combination of nucleotides and any nucleotides as small as dinucleotides, therefore it is not clear how does a targeted deletion plants in a region of a gene would have been produced without knowing the specific targets.
Similar recitation of the term “genomic locus is unknown” and “causative gene or region is located within an endogenous genomic locus” also present in claims 15 and 17 therefore the claims are also indefinite.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
Anticipated by Zhao et al.
Claims 1-5, 7-9 and 11-16 are rejected under 35 U.S.C. 102 (a) (1) as being anticipated by Zhao et al. (Published online: May 23, 2018, Journal: Nature Communications, Volume: 9, Issue: 2039, pages: 1-12) and as evidenced by Jia et al. (Published: 2008, Journal: MPMI 21 (4): 396–403. doi:10.1094/MPMI -21-4-0396).
Claims are drawn to a method of fine mapping a desired trait caused by a gene or region in a genomic locus having low intrinsic recombination frequency comprising: production and screening of targeted deletion plants. The claims are further drawn to the deletion is caused by TALEN or CRISPR associated nuclease etc.
Regarding claims 1, 2 , 13 and 14, Zhao et al. teaches a method of mapping a desired native broad spectrum blast resistant trait in rice (page 1, Abstract). Zhao et al. teaches the Ptr gene was identified in a fast neutron induced mutant (M2354) of rice variety Katy that still carries Pi-ta, but is susceptible to M. oryzae strains with AVR-Pita and subsequent analysis of a genetic cross between Katy and M2354 revealed a linked locus, Ptr, located in a linkage block near the centromere of Chromosome 12 and is presumably required for both Pi-ta and Pi-ta2 mediated disease resistance (page 2, left paragraph 2) and it is part of Pi-ta resistance complex (page5, left paragraph 1). Zhao et al. teaches Pi-ta is physically close to Ptr on a chromosomal region lacking recombination (page 10, left paragraph 2) or suppressed recombination (page 2, left paragraph 2).
Thus Zhao et al. identifies the previously unknown locus near centromere where the recombination is rare using mutation induced by fast neutron. Then Zhao et al. maps the Ptr locus using the site-specific deletion of the endogenous genomic locus of Katy near the previously known Pi-ta locus using CRISPR/Cas9, showing its importance of mapping a gene in recombination suppressed region where Pi-ta is located.
Furthermore, Jia et al. teaches Pi-ta gene is 1.39 MB away from the centromere of chromosome 12, therefore the recombination suppression occurs at this region (page 401, left paragraph 2). Jia et al. teaches they were unable to separate the Pi-ta gene from Ptr(t) in a series of crosses, including the use of 2,000 F2 progeny from a segregating population derived from a cross of Pi-ta/Ptr(t) with pi-ta/ptr(t) homozygotes showing intense recombination suppression (page 401, left paragraph 2).
Furthermore, applicant defines “A "low intrinsic recombination frequency" refers to a low number of recombination events identified based on the genetic map distance in a given region” (Spec, page 10, paragraph 00048). Since there is no limit what does low number of recombination events would mean, it would be relative to the recombination rates of particular locus or organisms and it does not provide any valid limit of lower or upper limit. Therefore, any relative frequency lower than 50% can be considered low relative frequency.
Zhao et al. teaches their method comprises targeted deletion of Ptr gene in Katy cultivar using two gRNA spacers that span 811bp in the third exon of the gene, where the resulting polycistronic tRNA-gRNA gene was introduced into pRGEB32 vector and Rice Calli from rice variety Katy were transformed with binary vector Agrobacterium tumefaciens where the Chromosomal deletions were detected by PCR with primers flanking the two target sites of each gene (page 10, right last paragraph).
Zhao et al. teaches two sequence-specific guide RNAs (gRNAs) were designed to disrupt the Ptr gene sequence in the third exon in front of the 2 bp deletion (i.e. GG) or region around it as found in M2354 (page 2, right last and second paragraphs). Thus, use of two sgRNA would have two deletions in the Pi-ta locus near or in the Ptr gene as also showed by Figure 2a below where there is presence of different deletion sizes in the LOC_Os12g18729 locus of Pi-ta resistance complex. Furthermore, Figure 2A showed for example 1B/C a does not comprise deletion in the GG region wherein the line 2-A/D a comprise the GG deletion.
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Targeted deletion at the endogenous LOC_Os12g18729 locus using CRISPR/Cas9 resulted in 34 plant from four independent events that carry deletion of 810bp between the two target sites (page 2 and 3, last and first paragraph, Figure 2A), wherein each plant for example in asterisk in Figure 2A shows a site specific deletion. Figure 2 showed the Cas9 editing resulted in InDels of differing length or a fragment deletion between the two protospacer (PS) sites are indicated by asterisk (*). Figure 2C and 2D further showed (see figure below) that each of the mutant 1Bm 2A, 2D, 3G and 3Q had higher disease rating than the resistant line Katy so each of the combination of deletion has different resistant phenotypes to each of the IC-17 and IB-49 blast races, further showed in Supplementary Figure 2.
The increase in disease rating or susceptibility in the targeted deletion plants as compared to parent Katy shows the Ptr is a causal gene for the disease resistance or it is the region for native broad spectrum blast resistance gene and each site-specific deletion is deletion of the Katy genomic sequence that is native to the Katy line.
Zhao et al. confirms in comparison with Katy, CRISPR-edited ptr mutants with different deletions sizes exhibited a much larger lesion area and had a higher disease rating with both spray- and spot-inoculations, therefore, the targeted mutation of Ptr in the resistant Katy cultivar led to disease susceptibility to avirulent isolates, further confirming that Ptr is required for rice blast resistance (Fig. 2b–d and Supplementary Figs 2 and 3). Zhao et al. further showed in Figure 2c and 2d (see below) the different deletions sizes had different effect to the two different isolates of blast disease (i.e. isolates IC-17 and IB-49) showing different phenotypic effect of the infection of the blast races on different deletion sizes in different regions of endogenous LOC_Os12g18729 locus.
Zhao et al. concludes the targeted mutation of Ptr in the resistant Katy cultivar led to disease susceptibility to avirulent isolates, further confirming that Ptr is required for rice blast resistance where Ptr gene function as new gene independently of the previously known Pi-ta gene (page 3, left paragraph 1 and 2).
Zhao et al. teaches targeted mutation of Ptr in a resistant cultivar using CRISPR/Cas9 leads to blast susceptibility, further confirming its resistance function (page 1, Abstract). Hence clearly showing the method of targeted mutation which is deletion by CRISPR/Cas9 confirmed the resistance function of Ptr gene as new gene.
Thus Zhao et al. teaches a method for mapping a blast disease resistance trait (i.e. desired trait) caused by Ptr gene region which has low intrinsic recombination frequency, comprising:
Providing a rice plant line (i.e. line Katy) comprising a causative gene or region as Ptr gene for a native trait of blast resistance, wherein the Ptr is located with the endogenous locus of chromosome 12 as Pi-ta resistance complex of the line Katy and the region is near to centromere and has low intrinsic recombination frequency.
introducing at least two different site-specific deletions by using two specifically designed gRNA at endogenous genomic locus of chromosome 12 Pi-ta resistance complex in a plurality of plants of line Katy, thereby creating a plurality of targeted deletion plants, wherein each targeted deletion plant comprises one of the site-specific deletions at the locus and wherein the locus comprises the causal gene for blast disease resistance or region for a native trait of blast disease resistance and each site-specific deletion is a deletion of genomic sequence in chromosome 12 in Pi-ta resistance complex that is native to the plant line katy;
screening the targeted deletion plants for an increase or decrease in a phenotype of the desired native trait of blast resistance;
confirming which of the site-specific deletions causes the increase or decrease in the phenotype, thereby mapping the genomic location of the native trait as showed in figure 2C and 2D.
Regarding limitation of location of the causative gene or region within the endogenous genomic locus was unknown. Zhao clearly showed the targeted deletion of the endogenous genomic locus of Katy in Pi-ta resistance complex further fine map the genomic region of Pi-ta leading to the identification of Ptr gene. Applicant has not added any method step that would make the method step different when the causative gene or region within the genomic locus was unknown. Therefore, just statement of the causative gene was unknown does not make the method step novel. Zhao showed all the recited method steps. Furthermore, for example Zhao uses two guide RNAs which causes deletion in two different regions which not only target the previously identified “GG” region of the third exon but also targets regions around it and showed the deletion still causes the increase in disease ratings (see Figure 2A for line 1B/C a and b). Furthermore the other lines from 2A/D, 3A, etc. showed different size of deletions leading to difference in response to inoculation of different blast races (see Figure 2 and supplementary Figure 3).
Regarding 3, Zhao et al. teaches selecting plant having the targeted deletion using PCR restriction enzyme assay where 34 plants from four independent events were obtained (page 2, last right paragraph) wherein the progeny from the CRISPR-edited mutants were inoculated with two avirulent races (isolate), IB-49 (ML1) or IC-17 (ZN57), of M. oryzae carrying AVR-Pita (page 3, left paragraph 1) that showed increase in disease rating (Figure 2C).
Regarding claim 4, Zhao et al. teaches the edited Ptr locus is located in a linkage block near the centromere of Chromosome 12 and (page 2, left paragraph 2).
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Regarding claims 5 and 16, Zhao et al. teaches Pi-ta is physically close to Ptr on a chromosomal region lacking recombination (page 10, left paragraph 2) or suppressed recombination (page 2, left paragraph 2).
Regarding claims 7, 9, and 11, Zhao et al. confirms in comparison with Katy, CRISPR-edited ptr mutants with different deletions sizes exhibited a much larger lesion area and had a higher disease rating (i.e. plant health related trait) with both spray- and spot-inoculations, therefore, the targeted mutation of Ptr in the resistant Katy cultivar led to disease susceptibility to avirulent isolates, further confirming that Ptr is required for rice blast resistance (Fig. 2b–d and Supplementary Figs 2 and 3).
Regarding claim 8, the SgRNA would have the target that would have partial sequence.
Regarding claim 15, Zhao et al.’s method confirms that Ptr is required for rice blast resistance (Fig. 2b–d and Supplementary Figs 2 and 3).
Regarding claim 12, Zhao et al. Figure 2 above showed different deletion mutants and CRISPR-Cas9 causes double strand break.
Hence Zhao et al. anticipates claims 1-5, 7-9 and 12-16.
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.
The factual inquiries for establishing a background for determining obviousness under 35 U.S.C. 103 are summarized as follows:
1. Determining the scope and contents of the prior art.
2. Ascertaining the differences between the prior art and the claims at issue.
3. Resolving the level of ordinary skill in the pertinent art.
4. Considering objective evidence present in the application indicating obviousness or nonobviousness.
This application currently names joint inventors. In considering patentability of the claims the examiner presumes that the subject matter of the various claims was commonly owned as of the effective filing date of the claimed invention(s) absent any evidence to the contrary. Applicant is advised of the obligation under 37 CFR 1.56 to point out the inventor and effective filing dates of each claim that was not commonly owned as of the effective filing date of the later invention in order for the examiner to consider the applicability of 35 U.S.C. 102(b)(2)(C) for any potential 35 U.S.C. 102(a)(2) prior art against the later invention.
Obvious over Zhao et al. and further in view of Li et al.
Claims 1 and 6 are rejected under 35 U.S.C. 103 as being unpatentable over Zhao et al., and further in view of Li et al. (Published: 2016, Journal: Nature plants 2:1-7).
Claims are drawn to a method of fine mapping a desired trait caused by a gene or region in a genomic locus having low intrinsic recombination frequency comprising: production and screening of targeted deletion plants. The claims are further drawn to a method wherein the low recombination is due to lack of homology to wild type chromosomes.
Regarding claim 1, Zhao et al. teaches the targeted deletion of the endogenous genomic locus of Katy in Pi-ta resistance complex further fine map the genomic region of Pi-ta leading to identification of Ptr gene with low intrinsic recombination because of its presence near to centromere. Zhao et al. teaches the method of screening the deletion plants and confirming the deletions, see analysis above.
Regarding claim 6, Zhao et al. specifically does not teach wherein the low recombination is due to lack of homology to wild type chromosomes.
Li et al. (Published: 2016, Journal: Nature plants 2:1-7) teaches deletion of several haplotypes causes the recombination suppression in common primrose due to lack of homology between different floral morphology (Primula vulgaris) (page 1, Abstract, Figure 2 and 3, see figure 3 below).
Therefore, someone skilled the art would delete such haplotypes in primrose as the method taught by Zhao et al. effective for discovering new genes in a gene complex with low intrinsic recombination leading to increase in recombination by increased homology to region in the same interval on wild type chromosome that lack the unique haplotype.
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Obvious over Zhao et al. and further in view of Cannon et al.
Claims 1 and 10 are rejected under 35 U.S.C. 103 as being unpatentable over Zhao et al., and further in view of Cannon et al. (Published: 2012, Journal: Breeding Science 61: 437–444).
Claims are drawn to a method of fine mapping a desired trait caused by a gene or region in a genomic locus having low intrinsic recombination frequency comprising: production and screening of targeted deletion plants. The claims are further drawn to a method wherein the low recombination is due to lack of homology to wild type chromosomes.
Regarding claim 1, Zhao et al. teaches the targeted deletion of the endogenous genomic locus of Katy in Pi-ta resistance complex further fine map the genomic region of Pi-ta leading to identification of Ptr gene with low intrinsic recombination because of its presence near to centromere. Zhao et al. teaches the method of screening the deletion plants and confirming the deletions, see analysis above.
Regarding claim 10, Zhao et al. does not teach the causal gene or region exhibits either increased or decreased soybean protein concentration.
Cannon et al. teaches a prominent feature in the soybean genome is the large, distinct pericentromeres in all of the chromosomes which are repeat-dense and gene-poor, and have extremely suppressed rates of recombination. Cannon et al. teaches ~1/5th of the gene complement occurs in regions of the genome that only rarely recombine and this has consequences for QTL mapping of traits in this region, and for attempts to break linkages between desirable and undesirable traits in the pericentromere (pages 439 and 440, last and first paragraphs). Cannon et al. teaches one such example is the soybean seed protein QTL on linkage group I (LG I / Gm20) which flanked by two non-segregating markers, nevertheless spans ~8.4 Mbp in Gm20 because it is located within a pericentromere (page 440, left paragraph 1).
Thus it would have been obvious before the effective date of filing of the invention for a skilled in the art to apply known technique in rice plant to fine map new causal gene or region within a genomic locus with low intrinsic recombination frequency and use it for finding such genes or regions for finding genes related to protein concentration as taught by Cannon et al. that QTL are present for soybean seed protein flanked by non-segregating markers near centromere, that would lead to the invention wherein the method can be utilized for fine mapping soybean protein concentration genes found in the pericentromeric region that would lead to increase or decrease of soybean protein concentrations.
Obvious over Zhao et al. and further in view of Jia et al.’09.
Claims 17-20 are rejected under 35 U.S.C. 103 as being unpatentable over Zhao et al., and further in view of Jia et al.’09 (Published: 2009, Journal: Heredity 103: 333–339).
Claims are drawn to a method of fine mapping a desired trait caused by a gene or region in a genomic locus having low intrinsic recombination frequency comprising: production and screening of targeted deletion plants. The claims are further drawn to the method further comprises crossing the modified plant with a recurrent parent and screening progenies.
Regarding claim 17, Zhao et al. teaches the targeted deletion of the endogenous genomic locus of Katy in Pi-ta resistance complex further fine map the genomic region of Pi-ta leading to identification of Ptr gene with low intrinsic recombination because of its presence near to centromere. Zhao et al. teaches the method of screening the deletion plants and confirming the deletions, see analysis above.
Zhao et al.’s method of deletion would produce novel haplotype since it has deletion in more than one place (see Figure 2 a above).
Zhao et al. does not teach backcrossing and screening of progenies.
The crossing and modified plant to recurrent parent and screening for difference in trait in the progeny of the cross is known in the art.
Jia et al.’09 teaches introgression of chromosome fragment around the rice blast resistance Pi-ta gene using backcross wherein in the BC5F2 generations generated from donor parent M202 and recurrent parent Katy, the genomic fragments around Pi-ta ranging from half (14Mbp) to the entire chromosome (27Mbp) were found from the donor (i.e. Katy (page 333, Abstract, Figure 1 for backcross procedure). Jia et al.’09 teaches the screening the BC5F1 for resistance to blast and showed the difference in the resistance and susceptibility (page 334, Table 1).
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Therefore, someone skilled in the art would use the known method of backcrossing to the modified plant to screen for the different in traits leading to know the loss or gain of desired traits in the backcross progeny.
Regarding claim 18, Zhao et al. Figure 2 a showed there are at least 2 site specific deletions.
Regarding claims 19, Zhao et al. teaches Pi-ta is physically close to Ptr on a chromosomal region lacking recombination (page 10, left paragraph 2) or suppressed recombination (page 2, left paragraph 2).
Regarding claim 20, Zhao et al. confirms in comparison with Katy, CRISPR-edited ptr mutants with different deletions sizes exhibited a much larger lesion area and had a higher disease rating (i.e. plant health related trait) with both spray- and spot-inoculations, therefore, the targeted mutation of Ptr in the resistant Katy cultivar led to disease susceptibility to avirulent isolates, further confirming that Ptr is required for rice blast resistance (Fig. 2b–d and Supplementary Figs 2 and 3).
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 17-20 are provisionally rejected on the ground of nonstatutory double patenting as being unpatentable over claims 1, 4 and 9 of copending Application No. 18840944 (Hereafter referenced as Application ‘944) in view of Jia et al.’09.
Regarding claims 17-19, Application ‘944 claim 1 recite a method of targeting a low recombinogenic pericentrometic chromosomal segment in a chromosomal art of a plant cell to rearrange the chromosomal arm by introducing one or more site specific DNA breaks in one or more chromosomal segment.
Application ‘944 claim 4 recite DNA breaks are targeted double strand breaks.
The rearrangement would have created novel haplotype in the genomic locus.
Application ‘944 claim 9 recite the rearranged chromosomal segment comprise one or more QTL or alleles associated with an agronomic trait that were previously not associated with such traits dues to low observable recombination frequency.
Jia et al.’09 teaches introgression of chromosome fragment around the rice blast resistance Pi-ta gene using backcross wherein in the BC5F2 generations generated from donor parent M202 and recurrent parent Katy, the genomic fragments around Pi-ta ranging from half (14Mbp) to the entire chromosome (27Mbp) were found from the donor (i.e. Katy (page 333, Abstract, see Figure 1 above for backcross procedure). Jia et al.’09 teaches the screening the BC5F1 for resistance to blast and showed the difference in the resistance and susceptibility (page 334, Table 1).
Therefore, someone skilled in the art would use the known method of backcrossing to the modified plant to screen for the different in traits leading to know the loss or gain of desired traits in the backcross progeny.
Regarding claim 20, Application ‘944 claim 1 recite finding the modified plant to be stable and he rearranged chromosomal segment is heritable in one or more progeny population which encompass selecting the modified plant.
This is a provisional nonstatutory double patenting rejection.
Summary
No claim is allowed.
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/SANTOSH SHARMA/ Examiner, Art Unit 1663
/DAVID H KRUSE/ Primary Examiner, Art Unit 1663
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