DETAILED ACTION
Notice of Pre-AIA or AIA Status
1. The present application is being examined under the pre-AIA first to invent provisions.
Status of the Application
2. Claims 49, 51-68, 70, 71, 73-76, and 78 are pending.
3. Claims 66 and 67 remain withdrawn.
4. Claims 49, 51-65, 68, 70, 71, 73-76, 78 are examined.
Continued Examination Under 37 CFR 1.114
5. A request for continued examination under 37 CFR 1.114, including the fee set forth in 37 CFR 1.17(e), was filed in this application after final rejection. Since this application is eligible for continued examination under 37 CFR 1.114, and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114. Applicant's submission filed on April 1, 2026 has been entered.
Election/Restrictions
6. Applicant's election with traverse of Group I, claims 49-65, in the reply filed on June 19, 2017 is acknowledged. In the Non-Final Office Action mailed on July 13, 2017, the traversal was not found persuasive and the requirement was therefore made FINAL. Claims 66 and 67 remain withdrawn from further consideration pursuant to 37 CFR 1.142(b), as being drawn to a nonelected Invention, there being no allowable generic or linking claim. Applicant timely traversed the restriction (election) requirement in the reply filed on June 19, 2017. Given that the previously added claim 78 would have been included in the elected group, it was examined.
Claim Interpretation
7. The following is noted with regard to claim interpretation. In the previous amendments, Applicant added the following limitation to claim 49: “the AHASL polynucleotide being free of site-directed mutation.” The structure of a polynucleotide is determined by its nucleotide sequence. Any function, such as the ability to encode a specific polypeptide is inherent in said sequence. The manner in which said polynucleotide was obtained does not affect its structure and, therefore, patentability. It is noted that “[E]ven though product-by-process claims are limited by and defined by the process, determination of patentability is based on the product itself. The patentability of a product does not depend on its method of production. If the product in the product-by-process claim is the same as or obvious from a product of the prior art, the claim is unpatentable even though the prior product was made by a different process." In re Thorpe, 777 F.2d 695, 698, 227 USPQ 964, 966 (Fed. Cir. 1985). MPEP 2113.
In the instant case, whether the claimed “mutagenized” AHASL polynucleotide was obtained using “site-directed” mutagenesis or another method, does not affect the structure of said polynucleotide. In the instant claim 49, said structure is determined only by the nucleotide sequence and the inherent ability of said polynucleotide to encode a mutant AHASL protein comprising the two recited substitutions.
Claims 70 and 71 are given their broadest reasonable interpretation as encompassing the plant of claim 49 comprising a detectable amount of the herbicide on any portion of the plant. The term “no injury,” in claim 71, is interpreted as encompassing the absence of any kind of herbicidal injury, however determined, on any portion of the plant. The term is not defined in the specification.
Response to Arguments
Applicant takes issue with Examiner’s claim interpretation and reiterates the argument based on the regulatory regimes that apply to transgenic and non-transgenic plants in the US and abroad. Applicant also argues as follows: “Because of these real-world differences between the three manner-of-making agricultural product segments, a seed or plant containing the exact same gene variants - made by traditional/mutagenized, GM, or GE techniques - and with no difference in morphology or molecular structure are not identical products in the real world strictly and only because of their method of making.” (page 7 of the Remarks).
This is not found to be persuasive. Regulatory issues and other business considerations are not relevant to the analysis on which the instant rejection is based. If there is no “difference in morphology or molecular structure” between a claimed product and a product that was disclosed or made prima facie obvious by the prior art, that claimed product is not patentable under 35 U.S.C. 102 or 103. It is also noted that the instant claims interpretation deals with the structure of a polynucleotide, not a plant.
Applicant cites MPEP 2113 and In re Thorpe and other legal precedent from said section and argues as follows: “None of these precedential cases addressed seeds or plants nor any technology invoking one or more of the three agricultural product segments, nor any field in which the method-of-making defines the product or its permissible uses. Instead, these precedents addressed chemical, biochemical, medical, and material technologies for which their manner of making presents no real-world difference. Thus, a given structure in any of these technology categories is fungible with every identical structure, regardless of its manner of making. That is the fundamental basis for - and underlying assumption of - the precedential decisions that the MPEP relies on, and thus that is the fundamental basis for the MPEPs summary of the same. Yet, that underlying assumption is invalid in and does not apply to the field of seeds and plants” (page 8 of the Remarks).
First, the court’s statement in In re Thorpe that states that “the determination of [a product’s] patentability is based on the product itself” and not its method of production, is not an “underlying assumption” of that case but its express holding and a controlling legal precedent. The is no evidence that it excludes any products, such as nucleic acids or plants. Second, the issue in the instant claim interpretation is not the structure of a plant but a polynucleotide. The Examiner maintains that the structure of a polynucleotide is determined by its nucleotide sequence and not its method of making. This is entirely consistent with In re Thorpe and other controlling precedent.
Applicant argues as follows: “As one of ordinary skill in the field of agriculture understands, as mentioned above, two structurally identical seeds - wherein one is a traditional/mutagenized product and the other is a transgenic/GM or GE product - are actually different products in the real world, with different scope of uses, et al. Their different manners of making determine each product's identity … In the present case, the fact that the claimed plant was produced by traditional mutagenesis, and without site-directed mutation or transgenesis, defines the manner-of-making element that renders the claims distinct from the prior art” (pages 8-11 of the Remarks).
This is not found to be persuasive. First, as stated above, the term “free of site-directed mutation” refers to the AHASL polynucleotide, and not a plant or a seed. Second, to the extent that the argument is directed to the patentability of a plant, Applicant has failed to show how the patentability or a plant under the US statutes would be affected by any state regulatory regimes regarding transgenic or non-transgenic plants. The fact that a regulatory body may consider “two structurally identical seeds” to be “actually different products in the real world” is irrelevant to the patentability: if one of those identical seeds is claimed and the second one is disclosed or made obvious by the prior art, the first seed is not patentable. In the instant case, a plant comprising an endogenous AHASL polynucleotide encoding the AHASL polypeptide with the two claimed substitutions would have been prima facie obvious by the cited art.
A “relevant field” or a “class” in which Applicant may categorize the claimed invention does not affect nor address the substance of the Examiner’s claim interpretation, which interpretation is directed specifically to the structure of a polynucleotide recited in the claims. The Examiner maintains that the structure of a polynucleotide is determined by its nucleotide sequence, and not its method of production.
Claim Rejections - 35 USC § 103
8. The following is a quotation of pre-AIA 35 U.S.C. 103(a) which forms the basis for all obviousness rejections set forth in this Office action:
(a) A patent may not be obtained though the invention is not identically disclosed or described as set forth in section 102, if the differences between the subject matter sought to be patented and the prior art are such that the subject matter as a whole would have been obvious at the time the invention was made to a person having ordinary skill in the art to which said subject matter pertains. Patentability shall not be negatived by the manner in which the invention was made.
9. Claims 49, 51-65, 68, 70-71, and 73-76, and 78 remain rejected under pre-AIA 35 U.S.C. 103(a) as being unpatentable over Sala et al (WO 2007/005581, published January 11, 2007, filed on July 1, 2005) in view of Cheung et la (US Patent Publication 2004/0142353, published on July 22, 2004), Tan et al (Tan et al (Pest Manag. Sci. (2005) 61:246-257), Arntzen et al (US Patent 7,094,606, filed on August 5, 1997), and Penner et al (US Patent No. 5,859,348, issued January 12, 1999). Applicant's arguments filed on April 1, 2026 have been fully considered but they are not persuasive.
The claims are drawn to a non-transgenic Brassica napus plant comprising a mutagenized Brassica napus polynucleotide encoding an AHASL polypeptide having a threonine substitution at a position corresponding to position 122 of SEQ ID NO: 1 and an asparagine substitution at a position corresponding to position 653 of SEQ ID NO: 1; to a cell, plant part, or seed of said plant, and to a method of using said plant. The instant specification teaches that SEQ ID NO: 1 is the amino acid sequence of the AHASL from Arabidopsis.
Sala et al teach herbicide-resistant sunflower plants comprising nucleic acid sequences encoding a double-substituted mutant AHASL. The first mutation is A107T (in sunflower numbering), which corresponds to position 122 of the instant SEQ ID NO: 1, which represents the Arabidopsis AHASL (claim 19). The second mutation is an asparagine substitution at the relative position 638, which corresponds to the position corresponding to position 653 of the instant SEQ ID NO: 1 (claims 19 and 20). Sala et al teach an expression cassette comprising a promoter operably linked to the polynucleotide encoding the above double-mutated sunflower AHASL (claims 21-22; pg. 7, lines 13-14). Sala et al teach a method comprising the steps of transforming a plant cell with the expression cassette comprising a plant promoter, operably linked to a mutated polynucleotide, such as the double mutated one above; and regeneration a transformed plant from the transformed plant cell (pg. 7, lines 20-27). Sala et al teach that their invention could be used for transformation of any plant species, including Brassica napus (pg. 45, lines 10-29).
Sala et al teach a method comprising transforming a host cell the with a transformation vector comprising the polynucleotides of their invention, including the above double mutated AHAS; exposing the cell to a level of an imidazolinone herbicide that would kill or inhibit the growth of a non-transformed host cell, and identifying the transformed host cell by its ability to grow in the presence of the herbicide (pg. 9, lines 3-10; claims 19-23). Sala et al teach treating resistant seeds with seed treatment, which includes seed coating and comprises AHAS inhibiting herbicides such as imazapyr and imazethapyr, among others (paragraph spanning pg. 54 and 55). Sala et al teach methods of combating undesired vegetation, wherein the seeds of the resistant plants are contacted before sowing and/or after pregermination with an AHAS-inhibiting herbicide; Sala et al teach said method wherein the weeds include dicot weeds such as those from the genera Datura, Sinapis, and others. (pg. 56, lines 12-28). Sala et al teach applying herbicide in a composition with other herbicides and adjuvants (page 46, first full paragraph).
Sala et al teach that the regions of AHASL comprising the herbicide resistance mutations are conserved, and teach that “Using the AHASL sequences of the invention and methods known to those of ordinary skill in art, one can produce additional polynucleotides encoding herbicide resistant AHASL polypeptides having one, two, three, or more amino acid substitutions at the identified sites in these conserved regions.” (pg. 62, lines 13-28; Table 4). Sala et al teach, at SEQ ID NO: 13 and 14, a nucleic acid and an amino acid sequence of the wild-type AHASL from Arabidopsis thaliana (see Sequence Listing on pg. 12-13 and following the Drawings).
Sala et al teach the sunflower plants comprising the A122T mutation showed resistance to imazamox at up to 300 g ai/ha; and that very little injury was observed at the highest rate doses of imazamox and imazapyr (Example 5 on pg. 60-61; Fig. 3 and 5). Sala et al teach crossing the herbicide resistant plants of their invention with a second plant that is not resistant to said herbicide and obtaining resistant progeny (paragraph spanning pages 46 and 47). Sala et al teach that herbicides could be used in a wet or dry formulation, and applied using spraying or dusting (pg. 46, lines 12-18).
Sala et al do not expressly teach a Brassica napus plant comprising said double-mutated AHASL comprising the above mutations.
Cheung et al teach Brassica napus plants comprising the “PM1” mutation in AHAS1 and methods of detecting a mutation resulting in said substitution in a plant (Abstract; Examples 4-6). Cheung et al teach that the mutation confers “commercially relevant imidazolinone tolerance” to the canola plants (Abstract; paragraph 11; Figures 4 and 5).
Tan et al teach that “PM1” is a canola mutation resulting in the S653N substitution. Tan et al teach that it is one of the two known substitutions in canola (the other one being W574L or “PM2”) confers high levels of imidazolinone tolerance and has been used commercially since 1995 (Table 2; paragraph spanning pages 249-250). Tan et al teach that PM1 confers tolerance to imidazolinones only and can be stacked with PM2 (page 250, left col.). Tan et al teach that “Mutations at Ala122 and Ala205 exhibit acceptable tolerance to imidazolinones and are also a good choice for the development of imidazolinone-tolerant crops” (page 248, right col.).
Arntzen et al teach an oligonucleotide-based method of making a localized point mutation in a plant cell, including a canola, soybean, potato, cotton, or tomato cell, to an AHAS gene causing the plant to be herbicide resistant (Arntzen et al, claim 1; col. 8, line 32 - col. 9, line 3). Arntzen et al teach regenerating a plant from said resistant cells and obtaining seeds and progeny of said plant (claims 1-8). Arntzen et al teach that using the method, a mutation may be introduced into any allele of the AHAS gene (col. 8, lines 46-48).
Penner et al teach sugar beet plants comprising a nucleic acid sequence encoding a mutated AHASL comprising two mutations: A113T (in sugar beet; 122 in Arabidopsis) and P188S (in sugar beet; 197 in Arabidopsis) (Penner et al col. 9, lines 35-55). Penner et al teach that said double mutation provides enhanced resistance to a combination of sulfonylureas and imidazolinones (Penner et al, col. 9, lines 56-59; Fig. 4). Penner et al teach that the resultant resistance is synergistic when compared to the level of resistance afforded by the two mutations individually (Penner et al, col. 10, lines 9-14; Table 2 in col. 10).
At the time the invention was made, it would have been prima facie obvious to use the mutagenesis method of Arntzen et al to introduce, using the sequence information taught by Sala et al, the S653N (PM1) substitution (taught by Sala et al, Tan et al, and Cheung et al) together with The A122T substitution (taught by Sala et al and Tan et al) onto the AHASL gene of any of the agriculturally significant species, including Brassica napus. It would have been obvious to use the resultant plant in a standard method of controlling undesired vegetation, including the method of Sala et al, wherein the plants are treated with an imidazolinone herbicide, including imazamox, imazethapyr, or imazapic. It would have been obvious to apply the herbicide in composition with an additive, such as adjuvant, and to apply said herbicide to a dicot weed, such as those taught by Sala et al. It would have been obvious to apply the herbicide in wet or dry formulation by spraying or dusting as taught by Sala et al.
It would have been obvious to use the seeds of resistant plants in a method of controlling undesired vegetation of Sala et al wherein the seeds are treated with an herbicide before sowing and/or after pregermination, wherein the herbicide is an imidazolinone, such as imazethapyr, imazamox, or imazapyr. It would have been also obvious, in view of the teachings of Sala et al and as a matter of standard industry practice, to use said method pre-emergence by applying an appropriate imidazolinone to the seeds of said resultant tolerant plants. The resultant prima facie obvious Brassica plant, when used in said method of weed control, would comprise “herbicide residue” and show “no injury,” at least on a portion of the plant, under the above claim interpretation.
Using the herbicide resistant plant in a breeding method, such as the method of Sala et al, to introgress herbicide resistance into a second plant would have been obvious as well.
It would have been obvious to use the S653N substitution, which was commercially used in canola at the time of filing, as taught by Tan et al and Cheung et al, in combination with another commercially used substitution, A122T.
One would have been motivated to do so because Sala et al expressly teach making sunflower plants comprising the two known point mutations, A122T and S653N, on the same AHASL protein, and teach applying their invention to any plant species, including canola. One would have been motivated to combine said two substitutions, specifically, on the AHASL of canola in view of the teachings of Tan et al and Penner et al, including the teachings of Penner et al that combining a mutation at position 122 with another point mutation results in a synergistic level of resistance to imidazolinones.
The specific levels of herbicide resistance to imidazolinones, including tolerance to 100 g ai/ha or 35 g ai/ha of imazamox would have naturally flowed from the prima facie obvious structure of said double-mutated AHASL and the plant comprising it. “The fact that appellant has recognized another advantage which would flow naturally from following the suggestion of the prior art cannot be the basis for patentability when the differences would otherwise be obvious.” Ex parte Obiaya, 227 USPQ 58, 60 (Bd. Pat. App. & Inter. 1985).
Moreover, given the teachings of Cheung et al, Penner et al and Sala et al, said levels would not have been unexpected, specifically given the teachings of Sala that the sunflower plants comprising the A122T mutation showed resistance to imazamox at up to 300 g ai/ha. Given the teachings of Penner et al, and the fact that both A122T and S653N substitution confer tolerance to imidazolinones, at least some degree of greater than additive tolerance to imazamox in the double mutant AHAS and the Brassica napus plant comprising it would not have been unexpected.
One would have had reasonable expectation of success in obtaining a plant resistant to imidazolinones, including imazamox or imazethapyr, given the conserved nature of the enzyme (as taught by Sala et al and Tan et al and well-known in the art), because the A122 and S653 residues are located within two of the five conserved AHASL regions, and given that Sala et al, Penner et al, and Arntzen et al successfully reduced their invention to practice. Given that the method of Arntzen et al does not involve the introduction of a transgene, the resultant plant would be considered non-transgenic.
Response to Argument.
Applicant reiterates the arguments directed to the individual references. Applicant argues that Sala “does not provide any teaching or guidance for how to obtain those multi-mutant AHASL” or to select A122T and S653N (pages 12-13 of the Remarks). Applicant argues that the teachings of Arntzen are “broad and prophetic,” only briefly mention “AHASL mutagenesis,” and do not suggest the combination of A122N and S653N in a Brassica plant (page 14). Applicant argues that Penner does not teach the claimed combination of substitutions in Brassica; and reiterates the argument directed to the teachings of Chong et al regarding the inactivation of a mutant AHASL (pages 14-15).
Applicant concludes as follows: “With no articulation of all the elements of the present claims and with no articulation of a basis upon which one of ordinary skill in the art could have formed a reasonable expectation of obtaining the presently claimed subject matter, the present rejection does not mount a prima facie case of obviousness. Thus, Applicants submit that the claimed invention is not obvious” (page 17 of the Remarks).
Applicant’s argument is not found to be persuasive. To the extent that the Remarks reiterate previously submitted arguments, those were addressed in detail in the previous Office Actions and remain not persuasive for the reasons of record.
For the articulation of specific reasons at to why one of ordinary skill in the art would have predictably arrived at the claimed invention with reasonable expectation of success Applicant is directed to the rejection above.
With regard to Sala, the Examiner maintains that Sala et al expressly teach making sunflower plants comprising the two known point mutations, A122T and S653N, on the same AHASL protein, and teach applying their invention to any plant species, including Brassica. Introducing those two mutations into an endogenous AHASL gene would have been obvious in view of the combined teachings of the cited art.
With regard to the teachings of Arnzen, the argument remains not persuasive for the reasons of record. The reference teaches and claims using the oligonucleotide-based method of making localized point mutations to introduce a mutation into an AHAS gene of a canola, soybean, potato, cotton, or tomato cell, causing the plant to be herbicide resistant (Arntzen et al, claim 1; col. 8, line 32 - col. 9, line 3). Contrary to Applicant’s position, the rejection above provides specific reasoning as to why one would have been able to use the method of Arntzen to arrive at the instantly claimed invention with reasonable expectation of success.
Regarding the teachings of Penner et al, and the fact that Penner deals with sugar beet and not Brassica, the previously submitted argument remains not persuasive either. The residues of AHAS taught in Penner are located the domains that are conserved in all of the crop species in which the enzyme has been studied (see Tan et al, Sala et al). Moreover, B. napus plants comprising the S653N substitution were known in the prior art at the time of filing (see Tan et al and Cheung et al).
Applicant’s teaching away argument, including the previously submitted argument based on the teachings of the Chong article remains not found to be persuasive. When evaluating a teaching away argument, "the nature of the teaching is highly relevant and must be weighed in substance. A known or obvious composition does not become patentable simply because it has been described as somewhat inferior to some other product for the same use.” In re Gurley, 27 F.3d 551, 553, 31 USPQ2d 1130, 1132 (Fed. Cir. 1994). MPEP 2145. At the same time, any evidence supporting patentability (including the evidence supporting a teaching away argument) must be weighed against evidence supporting prima facie case: each piece of rebuttal evidence should not be evaluated for its ability to knockdown the prima facie case. All of the competent rebuttal evidence taken as a whole should be weighed against the evidence supporting the prima facie case. In re Piasecki, 745 F.2d 1468, 1472, 223 USPQ 785, 788 (Fed. Cir. 1984). MPEP 716.01(d).
In the instant case, Chong et al do teach that in tobacco plants, the mutation of the serine at the relative position 653 (652 in the tobacco numbering) into asparagine inactivated the enzyme. However, this is far from being the only teaching regarding the S653N substitution. The Examiner maintains that at the time of invention, the substitution was not only well-known in the art and characterized in a number of crops, but used commercially, and in canola, specifically. See Tan et al, Cheung et al, above. The preponderance of the evidence thus outweighs Applicant’s teaching away argument based on Chong et al. Applicant’s argument fails to address or reconcile these teachings with Applicant’s position.
With regard to the recited property of herbicide tolerance, the Examiner maintains that there is no evidence in the record that the observed levels of the double mutant’s tolerance to imazamox were, in fact, unexpected. At the same time, the teachings of the prior art indicate that the recited property would not have been unexpected, at least under some conditions, all of which are encompassed by the claims. Sala et al, for example, teach that the sunflower plants comprising the A122T mutation alone showed resistance to imazamox at up to 300 g ai/ha; and that very little injury was observed at the highest rate doses of imazamox and imazapyr. Applicant’s argument fails to address these express teachings of Sala et al.
Moreover, with regard to the A122T and the combination of substitutions, Tan et al teach as follows: “Mutations at Ala122 and Ala205 exhibit acceptable tolerance to imidazolinones and are also a good choice for the development of imidazolinone-tolerant crops. … The majority of commercialized imidazolinone-tolerant crops are currently developed from either one or a combination of Ala205, Trp574, and Ser653 mutations. All commercialized imidazolinone-tolerant crops have been developed through selection or mutagenesis, utilizing conventional plant-breeding techniques, and are therefore non-transgenic” (page 248, right col.).
The Examiner maintains that the herbicide tolerance properties of both substitutions recited in the independent claim 49, A122T and S653N, were well-known in the prior art. Both residues, A122 and S653, as well as the domains in which they are located, are conserved in all crop species in which the enzyme has been studied. Moreover, their combination on the same AHASL molecule was also known: Sala et al expressly teach a double mutated AHASL polypeptide, comprising the two instantly claimed substitutions.
The one limitation that Sala et al do not expressly teach is a plant other than sunflower, such as Brassica napus, comprising said AHASL. Applicant’s invention thus amounts to introducing the two substitutions, each of which was well-characterized with regard to the herbicide resistance it confers, into another crop species. This would have been obvious and readily achievable using the methods available in the art at the time the instant invention was made. In addition, B. napus plants comprising the S653N substitution were commercially used at the time of invention (see Cheung et al, Tan et al, above). The rejection is maintained.
Conclusion
10. No claims are allowed.
11. All claims are identical to or patentably indistinct from, or have unity of invention with claims in the application prior to the entry of the submission under 37 CFR 1.114 (that is, restriction (including a lack of unity of invention) would not be proper) and all claims could have been finally rejected on the grounds and art of record in the next Office action if they had been entered in the application prior to entry under 37 CFR 1.114. Accordingly, THIS ACTION IS MADE FINAL even though it is a first action after the filing of a request for continued examination and the submission under 37 CFR 1.114. See MPEP § 706.07(b). Applicant is reminded of the extension of time policy as set forth in 37 CFR 1.136(a).
A shortened statutory period for reply to this final action is set to expire THREE MONTHS from the mailing date of this action. In the event a first reply is filed within TWO MONTHS of the mailing date of this final action and the advisory action is not mailed until after the end of the THREE-MONTH shortened statutory period, then the shortened statutory period will expire on the date the advisory action is mailed, and any nonprovisional extension fee (37 CFR 1.17(a)) pursuant to 37 CFR 1.136(a) will be calculated from the mailing date of the advisory action. In no event, however, will the statutory period for reply expire later than SIX MONTHS from the mailing date of this final action.
12. Any inquiry concerning this communication or earlier communications from the examiner should be directed to MYKOLA V KOVALENKO whose telephone number is (571)272-6921. The examiner can normally be reached Mon.-Fri. 9:00-5:30 PST.
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/MYKOLA V. KOVALENKO/ Primary Examiner, Art Unit 1662
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