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
Examiner acknowledges Applicants’ remarks made in response to the restriction requirement with respect to the underlying rationale for requiring restriction.
Claims 71-76 and 79 are withdrawn from further consideration pursuant to 37 CFR 1.142(b) as being drawn to nonelected inventions, there being no allowable generic or linking claim. Election for Group I and SEQ ID NO. 1 was made without traverse in the reply filed on 2/4/2026.
Priority
Applicant’s claim for the benefit of prior-filed application no. AU2021902650 filed 08/23/2021 and PCT/AU2022/050946 filed 08/22/2022 under 35 U.S.C. 119(e) or under 35 U.S.C. 120, 121, 365(c), or 386(c) is acknowledged.
Thus, the earliest possible priority for the instant application is August 23rd, 2021.
Information Disclosure Statement
The information disclosure statements (IDS) submitted on 9/23/2024, 8/18/2025, and 9/24/2025 were considered, initialed, and attached hereto. A signed copy of the list of references cited is included with this Office Action.
The listing of references on pages 74-76 of the Specification is not a proper information disclosure statement. For example, 37 CFR § 1.98(b) requires a list of all patents, publications, or other information submitted for consideration by the Office, and MPEP § 609.04(a) states, "the list may not be incorporated into the specification but must be submitted in a separate paper." Therefore, unless the references have been cited by the examiner on form PTO-892, they have not been considered.
Drawings
The drawings are objected to because they lack proper reference to SEQ ID NOs. Corrected drawing sheets in compliance with 37 CFR 1.121(d) are required in reply to the Office action to avoid abandonment of the application. Any amended replacement drawing sheet should include all of the figures appearing on the immediate prior version of the sheet, even if only one figure is being amended. The figure or figure number of an amended drawing should not be labeled as “amended.” If a drawing figure is to be canceled, the appropriate figure must be removed from the replacement sheet, and where necessary, the remaining figures must be renumbered and appropriate changes made to the brief description of the several views of the drawings for consistency. Additional replacement sheets may be necessary to show the renumbering of the remaining figures. Each drawing sheet submitted after the filing date of an application must be labeled in the top margin as either “Replacement Sheet” or “New Sheet” pursuant to 37 CFR 1.121(d). If the changes are not accepted by the examiner, the applicant will be notified and informed of any required corrective action in the next Office action. The objection to the drawings will not be held in abeyance.
Specification
The disclosure is objected to because it contains an embedded hyperlink and/or other form of browser-executable code. Applicant is required to delete the embedded hyperlink and/or other form of browser-executable code; references to websites should be limited to the top-level domain name without any prefix such as http:// or other browser-executable code. See MPEP § 608.01.
Status of Claims
Claims 66-85 are pending.
Claims 71-76 and 79 are withdrawn.
Claims 66-70, 77-78, and 80-85 filed 9/23/2024 are examined herein.
Claim Interpretation
The instant specification defines the term "atypical cinnamoyl-CoA dehydrogenase polypeptide 2" or "CAD2" refer as members of the short-chain dehydrogenase/reductase (SDR) family and states that examples of the CAD2 polypeptide family include polypeptides which share high primary amino acid sequence identity, for example at least 40%, at least 50%, at least 60%, at least 70%, least 80%, at least 90%, or at least 95% identity with the amino acid sequence of any one or more of SEQ ID NO's 1 to 10. This is taken to mean that the CAD2 is a member of the SDR family with >40% identity to the amino acid sequence of SEQ ID NOs 1-10.
Claim Rejections - 35 USC § 112(a)
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.
Claim 66, and claims 67-70, 77-78, and 80-85 depending therefrom, 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 claims contain 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. Claims 67-70, 77-78, and 80-85 are also rejected insofar as they depend from claim 66, and do not overcome the stated rejection(s).
The claims are broadly drawn to a plant having a genetically modified gene encoding an atypical CAD2 polypeptide, which, when expressed in the plant confers enhanced resistance to one or more biotrophic fungal pathogens(s).
The disclosure reduces to practice a resistance phenotype to Fusarium pathogens.
The instant disclosure does not reduce to practice that the expressed CAD2 polypeptide will confer resistance to any biotrophic fungal pathogen.
FCR resistance was evaluated in the instant specification using a highly aggressive strain of Fusaruim psudograminearum isolated from infected wheat crowns. FCR assessments were carried out in recombinant lines identified from fine-mapping the gene underlying FCR resistance at the 4HL locus Qcrs.cpi-4H. Transformation constructs were created from the full-length CDSs for each of the two candidate genes obtained from the predicted genes model of WBR1 for the resistant and susceptible lines. Barley was transformed with Agrobacterium-mediated transfer. The genes were cloned and characterized to find that, compared to the known protein structure of Mt-CAD2, which shares 64.15% sequence identity with the barley CAD2, there were four consecutive amino acid changes around the substrate binding site that likely led to changes in enzyme activity and thus resistance to FCR. Orthologs in other plant species, including wheat, rice, maize, and sorghum, were analyzed to provide resistance genes for these plant species, as well.
The instant disclosure does not reduce to practice resistance of other biotrophic fungal pathogens, which exhibit significant diversity in infection structure, host specificity, effector molecules, and genome structure. Janusz, G. et al. (2017, “Lignin degradation: microorganisms, enzymes involved, genomes analysis and evolution,” FEMS Microbiology Reviews, 41:941-962) teaches that some biotrophic fungi bypass typical host defenses, such as increased lignification [pg. 945, col. 1, ¶1]. For example, white-rot fungi degrade lignin through breaking down lignin-polysaccharide linkages to modify the structure and can survive in the soil for long periods of time [pg. 950, col. 2, ¶1]. Janusz teaches that other studies of microfungi (e.g. Penicillium chrysogenum, Fusarium solani and F. oxysporum) have shown lower degrees of lignin decomposition when compared to white rot fungi, although Fusarium has lignin-modifying peroxidases, as well [pg. 945, col. 1, ¶3]. Mapuranga, J. et al. (2022, “Infection Strategies and Pathogenicity of Biotrophic Plant Fungal Pathogens,” Front. Microbiol., 13:799396) teaches that other biotrophs rely on secreted effectors to manipulate the host immune system [Abstract], which may overcome the genetic modification of the instant application.
Additionally, claim 67 is broadly drawn to a plant having a genetically modified gene encoding an atypical CAD2 polypeptide comprising amino acids having a sequence at least 90% identical to the amino acid of SEQ ID NO. 1.
The instant disclosure reduced to practice SEQ ID NO. 1 with two particular amino acids that were highly conserved across homologs of the CAD2 polypeptide in barley which are indicative of altered function and thus provide the phenotype of Fusarium resistance.
The instant disclosure does not reduce to practice any sequence with 90% identity or more to SEQ ID NO. 1 to still confer enhanced resistance to one or more biotrophic fungal pathogens.
The instant disclosure describes HvCAD2, the Hordeum vulgare atypical CAD2 gene, encoding a predicted protein of 372 amino acids belonging to the SDR family [Example 3]. Within HvCAD2, four missense variants were detected at positions 542, 544, 547, and 551 between R and S alleles in the coding region of HvCAD2, which gave rise to four consecutive amino acid changes in polypeptides. These changes result in a change of amino acids from a conserved valine to alanine (position 179, V179A), isoleucine to leucine (position 180, I180L), valine to phenylalanine (position 181, V181F) and asparagine to threonine (position 182, N182T). The instant specification describes that the four consecutive amino acid changes around the substrate binding site would very likely lead to changes in enzyme activity of HvCAD2. The instant specification shows that the homologs of the gene in other plants had a valine at the position corresponding to amino acid 197 and an asparagine at position 182, demonstrating that these two amino acids were highly conserved in other CAD2 polypeptides.
SEQ ID NO. 1 is 372 amino acids long. 90% identity would allow for 37 mismatches to SEQ ID NO. 1. This may or may not include mutations of the necessitated two amino acids that were highly conserved across CAD2 homologs in other plants. A sequence with 90% identity to SEQ ID NO. 1 may or may not carry the same amino acids that were indicative of an altered function to provide the resistance phenotype to Fusarium. The specification does not provide enough evidence that the structure of such a sequence would provide the same function of enhanced resistance to one or more biotrophic fungal pathogens. Undue experimentation would be required to ensure that the difference in structure would still perform the function as claimed.
Examiner notes that defining the biotrophic fungal pathogen and CAD2 polypeptide sequence with more specificity may help to overcome this rejection.
Claim Rejections - 35 USC § 102
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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.
Claims 66 and 67 are rejected under 35 U.S.C. 102(a)(2) as being anticipated by Puzio, P. et al. “Plants with Increased Yield,” (US 20110277179 A1, published 11/10/2011).
Puzio teaches transgenic plants and/or transgenic plant cells comprising one or more nucleic acid(s), which enhances or improves one or more trait(s) of a transgenic plant [¶6]. Puzio teaches that yield-related traits concerning an improvement or increase of stress tolerance of a plant may be manifested by improving or increasing a plant's tolerance against stress [¶12]. Puzio teaches that the disclosed genes may be modified [¶660] (i.e., a plant having a genetically modified gene). Puzio discloses SEQ ID NO. 5269 with 90.3% identity to SEQ ID NO. 1 (alignment shown below).
The instant disclosure defines the atypical CAD2 gene as a member of the SDR family with >40% identity to the amino acid sequence of SEQ ID NOs 1-10. SEQ ID NO. 5269 has greater than 90.3% identity, meeting the sequence identity requirement based on the definition provided. SEQ ID NO. 5269 of Puzio has the claimed structure of 90.3% identity to SEQ ID NO. 1 and would therefore have the claimed function of claims 66 and 67. Having the required structure, the sequence taught by Puzio is deemed to read on the instantly claimed atypical CAD2, absent evidence to the contrary.
Query Match 90.3%; Score 1744; Length 339;
Best Local Similarity 98.8%;
Matches 335; Conservative 1; Mismatches 3; Indels 0; Gaps 0;
Qy 34 MAEKQRQGLNVEEGSSGAAGKLVCVTGASGYIASWIVKLLLDRGYTVHGTVRDTADPNKT 93
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 1 MAEKQRQGLNVEEGSSGAAGKLVCVTGASGYIASWIVKLLLDRGYTVHGTVRDTADPNKT 60
Qy 94 LHLRALDGANDRLHLFNANLLEEGSFDAAIDGCECVFHAASPVFFAAKDPKAELLDSAVS 153
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 61 LHLRALDGANDRLHLFNANLLEEGSFDAAIDGCECVFHAASPVFFAAKDPKAELLDSAVS 120
Qy 154 GTLNVLRSCKKASVRRVVITSSMASALFTGKPRTPDVIVDETWFSLPELCKKNQQWYTLS 213
||||||||||||||||||||||||| : |||||||||||||||||||||||||||||||
Db 121 GTLNVLRSCKKASVRRVVITSSMASVIVNGKPRTPDVIVDETWFSLPELCKKNQQWYTLS 180
Qy 214 KTLAEEAAWKFSKDNEQEIIVMNPTMVIGPLLQPTLNASVEAVLNLINGSSPTCPNYAHG 273
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 181 KTLAEEAAWKFSKDNEQEIIVMNPTMVIGPLLQPTLNASVEAVLNLINGSSPTCPNYAHG 240
Qy 274 WVNVRDVALAHILAYEVPSANGRYCIVERVAHYSELVKIICKMYPNIPLPDKCADDEPLF 333
||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Db 241 WVNVRDVALAHILAYEVPSANGRYCIVERVAHYSELVKIICKMYPNIPLPDKCADDEPLF 300
Qy 334 PTYQVSKDKIRSLGMELIPLETSIKETIESFKEKGFVAF 372
|||||||||||||||||||||||||||||||||||||||
Db 301 PTYQVSKDKIRSLGMELIPLETSIKETIESFKEKGFVAF 339
Claim Rejections - 35 USC § 103
In the event the determination of the status of the application as subject to AIA 35 U.S.C. 102 and 103 (or as subject to pre-AIA 35 U.S.C. 102 and 103) is incorrect, any correction of the statutory basis (i.e., changing from AIA to pre-AIA ) for the rejection will not be considered a new ground of rejection if the prior art relied upon, and the rationale supporting the rejection, would be the same under either status.
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 66, 68-70, 77-78, and 80-81 are rejected under 35 U.S.C. 103 as being unpatentable over Pan, H. et al. (2014), "Structural Studies of Cinnamoyl-CoA reductase and Cinnamyl-Alcohol Dehydrogenase, Key Enzymes of Monolignol Biosynthesis," The Plant Cell, 26:3709-3727 (as cited in IDSs filed 8/18/2025 and 9/24/2025), in view of Sawbridge, T. et al., “Manipulation of plant cell walls,” (AU 2011202252 B2, published 2/21/2013, as cited in IDS filed 9/23/2024), and Ma, Q. et al., (2017), "Contribution of both lignin content and sinapyl monomer to disease resistance in tobacco," Plant Pathology, 67:642-650.
Claim 66 recites a plant having a genetically modified gene encoding an atypical cinnamoyl-CoA dehydrogenase 2 (CAD2) polypeptide, wherein when expressed in the plant the polypeptide confers enhanced resistance to one or more biotrophic fungal pathogen(s) when compared to a corresponding plant lacking the gene.
Claim 68 recites the plant of claim 66, wherein the genetically modified gene is an exogenous polynucleotide encoding the polypeptide.
Claim 69 recites the plant of claim 66, wherein the one or more fungal pathogen(s) is a rot, rust or a mildew.
Claim 70 recites the plant of claim 66 which is a cereal plant or a legume plant.
Claim 77 recites a method of producing a plant with a genetic modification(s) of claim 66, comprising i) introducing a genetic modification(s) to a plant cell such that the cell is capable of producing an atypical cinnamoyl-CoA dehydrogenase 2 (CAD2) polypeptide that confers upon the plant comprising the cell enhanced resistance to one or more biotrophic fungal pathogen(s) when compared to a corresponding plant lacking the genetic modification(s),ii) regenerating a plant with the genetic modification(s) from the cell.
Claim 78 recites a method of producing a plant with a genetic modification(s) of claim 66, the method comprising the steps of i) crossing two parental plants, wherein at least one plant comprises a genetic modification(s) of claim 66, ii) screening one or more progeny plants from the cross in i) for the presence or absence of the genetic modification(s), and iii) selecting a progeny plant which comprise the genetic modification(s), thereby producing the plant.
Claim 80 recites a seed of the plant of claim 66, wherein the seed comprises the genetic modification(s).
Claim 81 recites a method of producing a plant part, the method comprising, a) growing a plant of claim 66, and b) harvesting the plant part.
Regarding claim 66, Pan teaches a functional and structural analysis of the enzymes cinnamoyl-CoA reductase (CCR) and cinnamyl alcohol dehydrogenase (CAD). Pan teaches that these enzymes catalyze the two key reactions in the conversion of cinnamic acid derivatives into monolignol building blocks for lignin polymers in plant cell walls [Abstract]. Pan teaches that lignin is a major structural component of cell walls and that it plays an important role in defense against pathogens [pg. 1, col. 1, ¶1]. Pan teaches that the polymeric structure of lignin forms from monolignols. The three prominent monolignols p-hydroxycinnamyl, coniferyl, and sinapyl alcohol, give rise to the lignin subunits hydroxycinnamyl (H), guaiacyl (G), and syringyl (S), respectively [pg. 1, col. 2, ¶1]. Pan teaches that atypical CAD has been shown to be involved in lignin biosynthesis in tobacco in prior studies, but belongs to the SDR family, unlike classic CAD enzymes [pg. 2, col. 2, ¶1].
Pan teaches atypical Medicago truncatula CAD2 mutants and the potential utility of engineered variants of Mt-CAD2 in modifying lignin content and composition in plants [pg. 3722, col. 1, ¶4]. Pan teaches that atypical Mt-CAD2 may compensate functionally upon the loss of the classic CAD enzyme as the classic CAD1 and the atypical CAD2 can catalyze the same reactions for lignin biosynthesis, but CAD2 has lower activity with the same substrates [pg. 3722, col. 2, ¶3]. For example, Pan teaches that engineered variants of Mt-CAD2 that exhibited enhanced activity with sinapaldehyde but decreased activity with coumaraldehyde and coniferaldehyde [pg. 3720, col. 1, ¶1]. Pan teaches the Mt-CAD2 binding site for the phenylpropene-aldehyde substrate and teaches that replacements of Mt-CAD2 large residues Tyr-136 and Ph2-226 with smaller residues Phe and Ala, resulted in increased catalytic activity against sinapaldehyde [pg. 3720, col. 1, ¶1]. This property could potentially be useful for promoting the production of sinapyl lignin (S-lignin) over guaiacyl lignin (G-lignin) [pg. 3722, col. 1, ¶4]. Pan teaches that such mutants could be introduced back into plants, particularly those harboring knockouts of the classic CAD enzyme to alter lignin composition.
Pan does not explicitly teach the atypical CAD2, wherein a plant having a genetically modified gene encoding the atypical CAD2 which, when expressed, confers enhanced resistance to biotrophic fungal pathogens.
However, Sawbridge teaches manipulation of plant cell walls though the modification of lignin biosynthesis [Abstract]. Sawbridge teaches that it is the final two reduction/dehydrogenation steps of the pathway, catalyzed by cinnamoyl CoA reductase (CCR) and cinnamyl alcohol dehydrogenase (CAD) that are considered to be specific to lignin biosynthesis [pg. 1, ¶1]. Sawbridge teaches that altered lignin composition may be desirable to improve disease resistance (i.e. enhanced resistance) [pg. 1, ¶1]. Sawbridge teaches CAD and CAD-like proteins and nucleic acids or nucleic acid fragments encoding amino acid sequences [pg. 1, ¶1] and introduction of genes encoding the polypeptides into perennial ryegrass for the production of transgenic plants, seeds or plant parts thereof (i.e. a plant having a genetically modified gene) [Example 6].
Although Pan and Sawbridge teach that atypical CAD2 may be mutated to modify lignin biosynthesis and a plant having a genetically modified gene encoding a CAD or CAD-like polypeptide which may confer disease resistance when expressed in the plant, Pan and Sawbridge do not explicitly teach that the atypical CAD2 confers enhanced resistance to biotrophic fungal pathogen(s).
However, Ma teaches that lignin has been suggested to play an important role in the place defense response to various pathogens. Ma teaches a series of transgenic tobacco lines that indicated that lower total lignin content aggravated the severity of tobacco black shank and bacterial wilt diseases [Abstract]. Ma teaches that both lignin content and S-lignin were positively correlated with disease resistance, demonstrating that both total lignin content and S-lignin content are main factors that contribute to the basic defense response in tobacco. Ma teaches that in prior studies the levels of S-lignin were increased in wheat upon stem rust fungus Puccinia graminis f.sp. tritici penetration (i.e. a rust biotrophic fungal pathogen) [pg. 643, col. 1, ¶2].
Given that Pan teaches mutant atypical CAD2 polypeptides which can modify the lignin content and composition, particularly S-lignin; given that Sawbridge teaches genetically modified plants having modified lignin biosynthesis-related genes, including CAD and CAD-like proteins and nucleic acids or nucleic acid fragments encoding amino acid sequences; and given that Ma teaches that lignin content and S-lignin content are primary components of pathogen defense, such as biotrophic fungal pathogens, it would have been prima facie obvious to one of ordinary skill at the time of filing to combine these teachings to create a genetically modified plant with enhanced resistance to one or more biotrophic fungal pathogens using the exogenous Mt-CAD2 mutants. One would have been motivated to do so as Pan teaches that atypical CAD2 mutants have utility in modifying lignin content and composition in plants, that Mt-CAD2 mutants exhibit enhanced activity with sinapaldehye, which promotes the production of S-lignin, and that lignin plays a large role in plant stress responses, such as pathogen attacks. Sawbridge additionally teaches that modifying lignin biosynthesis and the disclosed modifications may be used for disease resistance. Lastly, Ma teaches that lignin modification, particularly of S-lignin would aid in defense response against biotrophic fungal pathogens.
Regarding claim 68, Sawbridge teaches transformation vectors with chimeric lignin biosynthesis-related genes, such as CAD and CAD-like, using full-length open reading frame cDNAs of perennial ryegrass [Example 6]. Direct gene transfer experiments to tobacco protoplasts were performed using the transformation vectors under the control of the constitutive CaMV 35S promoter for production of transgenic tobacco plants (i.e. wherein the genetically modified gene is an exogenous polynucleotide encoding the peptide).
Regarding claim 69, Ma teaches that in prior studies the levels of S-lignin were increased in wheat upon stem rust fungus Puccinia graminis f.sp. tritici penetration (i.e. wherein the one or more fungal pathogens(s) is a rot, rust or mildew) [pg. 643, col. 1, ¶2].
Regarding claim 70, Sawbridge teaches that the vectors may be incorporated into a variety of plants, including monocotyledons (such as grasses from the genera Lolium, Festuca, Paspalum, Pennisetum, Panicum and other forage and turfgrasses, corn, oat, wheat and barley), dicotyledons (such as Arabidopsis, tobacco, 5 white clover, red clover, subterranean clover, alfalfa, eucalyptus) and gymnosperms (i.e. wherein the plant is a cereal or legume plant) [pg. 19, ln. 1-5].
Regarding claim 77, Sawbridge teaches that cells incorporating the vectors of the modified lignin genes may be selected and then cultured in an appropriate medium to regenerate transformed plants (i.e. a method of producing a plant with a genetic modification comprising introducing a genetic modification to a plant cell and regenerating a plant with the genetic modification) [pg. 19, ln. 16-20].
Regarding claim 78, Sawbridge teaches that the plants resulting from the genetic transformation may be reproduced, either sexually or asexually, using methods known in the art to produce successive generations of transformed plant (i.e. a method of producing a plant with a genetic modification comprising crossing two parental plants, wherein at least one plant comprises a genetic modification of claim 66) [pg. 19, ln. 22-25]. Sawbridge teaches that plants may be screened by methodology known to those skilled in the art and that nucleic acids or nucleic acid fragments according to the present invention and/or nucleotide sequence information thereof may be used as a molecular genetic marker for quantitative trait loci (QTL) tagging, QTL mapping, DNA fingerprinting and in marker assisted selection [pg. 9, ln. 10; pg. 15, ln. 15-20].
Regarding claims 80 and 81, Sawbridge teaches a plant seed or other plant part may be derived from the transgenic plant with the genetic modifications [pg. 20, ln. 10-15]. This indicates that the plant with the genetic modification is grown and a seed or plant part harvested therefrom.
By the rationale above for the plant of claim 66 having a genetically modified gene encoding a CAD2 polypeptide wherein when expressed in the plant, the polypeptide confers enhanced resistance to one or more biotrophic fungal pathogens, Pan, Sawbridge and Ma read on claims 68-70, 77-78, and 80-81. Although Pan, Sawbridge and Ma do not explicitly disclose screening or the progeny plants from a cross with the genetically modified plant, selecting the progeny, or harvesting the plant part, these aspects are implied and generally routine in the prior art.
Claims 82-85 are rejected under 35 U.S.C. 103 as being unpatentable over Pan, Sawbridge, and Ma, as applied to claims 66, 68-70, 77-78, and 80-81 above, and further in view of Palyi, L. Method and device for treating cereals and the like, (EP 0193840 A2, published 9/10/1986).
Claim 82 recites a method of producing flour, wholemeal, starch or other product obtained from seed, the method comprising; a) obtaining seed of a) obtaining seed of b) extracting the flour, wholemeal, starch or other product.
Claim 83 recites a product produced from a plant of claim 66 and/or a seed therefrom, wherein the product is a food product or beverage product.
Claim 84 recites a method of preparing a product of claim 83, the method comprising mixing seed, or flour, wholemeal or starch from the seed, with another food ingredient.
Claim 85 recites a method of preparing malt, comprising the step of germinating seed of claim 80.
Pan, Sawbridge and Ma teach the plant having a genetically modified gene encoding an atypical CAD2 polypeptide, wherein when expressed in the plant the polypeptide confers enhanced resistance to one or more biotrophic fungal pathogens. Sawbridge teaches obtaining a seed or plant part from a plant with the genetic modification. Pan, Sawbridge, and Ma do not teach a metho of producing flour or other product, food product or beverage product, or a method of preparing malt from the seed of claim 80.
However, Palyi teaches a method for peeling and grinding grain which is applicable to a wide variety of grains and seeds, including soft and hard wheat, durum wheat, barley, rye, malt barley, millet, African millet, milo, mung bean, sorghum and so on [pg. 1, ¶10]. Palyi teaches that, with the claimed apparatus, the lower disc, which rotates, has the advantage that the grains are not broken open during grinding, but rather a fractional treatment, which leads to an easy separation of the flour (i.e. a method of producing flour comprising extracting the flour) [pg. 3, ¶9].
Palyi additionally teaches that the casing left behind from the removal of the pericarp throughout the process can also be used for 100% germination for malt wheat (i.e. a method of preparing malt comprising the set of germinating the seed) [pg. 3, ¶5]. This has potential application in laboratories, in the baking industry and in brewing beer (i.e. a product produced from the plant of claim 66 or seed therefrom, wherein the product is a food product or beverage product).
Conclusion
No claims allowed.
Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to EMILY K. JOHNSON whose telephone number is (571)272-5761. The examiner can normally be reached Monday - Friday 7:30 am - 5:00 pm.
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/EMILY K JOHNSON/Examiner, Art Unit 1662
/BRATISLAV STANKOVIC/Supervisory Patent Examiner, Art Units 1661 & 1662