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 .
Claim Status
Claims 1-3, 5-8 & 24-26 are under examination on the merits.
Claims 4 & 9-23 are canceled.
Priority
Claims 1-3, 5-9 & 24-26 receive the U.S. effective filing date of 08/17/2021
Previous rejection of claim 3 under 35 U.S.C. 112(d) is withdrawn because claim 1 describes a representative of a plurality, rather than presenting the plurality as a limitation per se.
Previous rejection of claims 1-3, 5-9 & 24-26 under 35 U.S.C. 112(b) is withdrawn due to Applicant’s amendment to the claims.
Previous rejection of Claims 1-3, 5-9 & 24-26 under 35 U.S.C. 112(a) is withdrawn due to Applicant’s amendment to the claims.
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 1-3, 5-8 & 24-26 are rejected under 35 U.S.C. 103 as being unpatentable over Benson [Benson (2015) PLoS Genet 11(3) p.1-23; Published 04-12-2015] in view of Kerns [US20090064360; Published 03-05-2009].
Due to Applicant' s amendment of the claims, the rejection is modified from that set forth in the Office action mailed 17 Sep 2025, as applied to claims 1-3, 5-9 & 24-26. Applicant's arguments filed 17 Dec 2025 have been fully considered but they are not persuasive.
The claims are drawn to methods of increasing resistance to GLS in maize through detection of molecular markers associated with a disease resistance allele.
Benson teaches the presence of GLS resistance QTL on either distal end of chromosome 2 in maize [p.12, Fig.6; p.5, Table 2]. They indicate one of these two QTL is potentially more important for breeding purposes, specifically the ‘qGLS2.09’ QTL. They depict location of qGLS2.09 graphically (below, red outlined boxes), and present the estimated physical location of qGLS2.09 at 212,537,417–235,852,920bp:
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Benson teaches the physical location of the qGLS2.09 QTL at 212,537-235,852,920 [p.5, Table 2].
The importance of this region is highlighted specifically in the opening Abstract of Benson’s paper which points to three QTL of primary importance in GLS resistance, including qGLS2.09, which they state will have importance in breeding resistant varieties [p.1, Abstract].
Further, of the 16 QTLs represented in Benson’s comprehensive study of GLS, qGLS2.09 is specifically mentioned as one of only three alleles conferring disease resistance increases of more than 10%. Of the numerous QTL detected by Benson, only three were determined to be important enough to warrant fine mapping. One of those three is qGLS2.09 which was fine mapped from an original QTL size of 13Mb to 4Mb, estimated to contain 290 protein-coding genes, or targets for selection [p.11, par.1].
Benson teaches methods for GLS QTL identification [p.6, par.1] and the process of fine mapping underlying genes [p.11, par.1]. This includes genotyping (i.e. ‘screening the sample’) for the sequences associated with the QTL [p.16, ‘Analysis’]. They teach methods of crossing, using both ‘progeny plants’, as derived recombinant inbred lines (RILs), and included ‘parent plants’ used in producing the NILs in their mapping panel [p.15, ‘Plant Materials and Field Site’]. Absent evidence to the contrary, Applicant’s specific sequences, which are located at the distal end of chromosome 2, are simply a more granular, or higher-resolution, description of the sequences underlying Benson’s previously reported, known QTL for GLS resistance.
Benson does not teach Applicant’s exact sequence, which corresponds to the naturally occurring sequence in maize. Because Benson’s research utilizes a previously genotyped mapping panel, they also do not outline directly obtaining nucleic acid samples or selecting progeny. Benson does not describe the use of transgenic approaches to integrating the naturally occurring GLS resistance QTL they describe.
Kerns teaches methods of further identifying sequences within known GLS resistance QTL, as well as the specifics of marker-assisted-selection of Cercospora resistant maize plants.
Kerns teaches a method of genotyping/identifying, selecting, and crossing a maize plant carrying specific marker sequences [claims 1 & 2]. Kerns teaches the process of plant selection utilizing sequences/nucleotides (i.e. ‘selecting one or more’) [0086-0088], in both methods of marker-assisted selection (i.e. ‘obtaining a nucleic acid sample’) [par.116] and traditional plant breeding (i.e. ‘crossing a plant’, ‘selecting’, ‘producing a plant comprising a sequence’) [par.154].
Additionally, they describe how one would narrow a previously reported QTL to a more-specific (higher resolution) sequence comprising that QTL [0165]. Further, Kerns also points to additional guidepost markers or alleles conferring GLS resistance on chromosome 2, although they are not the exact sequences claimed by Applicant [0056].
Kerns teaches methods of introducing the claimed sequence via heterologous nucleic acid (i.e. transgenes) in their description of marker-assisted breeding directed to constructs and host-cells in maize (i.e. ‘introducing into the genome’, ‘a heterologous polynucleotide’, ‘a promoter’, ‘transgenic modification’, ‘wherein said plant is a monocot’) [par.148].
Introduction of transgenes utilizing Agrobacterium-mediated or biolistic-mediated methods is non-specific with regard to integration location of the transgene. Thus, Kerns’ teaching of the use of heterologous non-native constructs in conventional transgenic approaches [par.148] would inherently include integration into sites other than the native locus.
Before the effective filing date of the claimed invention, it would have been obvious to one of ordinary skill in the art to modify the known chromosome 2 GLS resistances taught by Benson for use in a breeding program as described in Kerns. The methods of such are outlined by Kerns, which could clearly be combined with the teaching of the genomic location and molecular details of GLS disease resistance locus taught by Benson.
Such GLS resistance QTL on chromosome 2 have been known in the art since the 19931, and Benson’s disclosure points directly to qGLS2.09 and highlights that specific QTL on chromosome 2 as warranting further investigation or fine mapping. It is routine in plant breeding to generate higher-resolution descriptions of valuable genomic locations or genes (i.e. fine mapping). In such instances, after the initial ‘discovery’ of valuable QTL, the task of further fine mapping the underlying gene or improved markers is generally limited only by the financial resources a research team has to genotype or phenotype recombinant lines. Such work is obvious, yet expensive.
One of ordinary skill in the art would have been motivated to combine these disclosures in order to further utilize the causative allele of the well-known, established GLS resistance in both traditional and transgenic breeding programs. They would want to do this because GLS is a well-recognized and globally significant challenge to maize yield. It is predictable that the known genes or alleles on chromosome 2 could be used to create more GLS resistant, and thus valuable, cultivars. Routine procedures of high-resolution mapping and MAS or transgenic breeding would be a way to potentially integrate the known disease resistances into susceptible maize backgrounds.
Referring to Applicant’s specification, the physical location of their claimed PRR QTL is reported to be 231,209,991-235,441,2327 with a peak correlation at 233,012,091 [specification, p.48, Table 6]. Applicant’s claimed sequence is directly and entirely within Benson’s previously reported qGLS2.09 QTL.
Absent evidence to the contrary, Applicant’s specific sequences, which are located at the distal end of chromosome 2, are simply a more granular, or higher-resolution, description of the sequences underlying Benson’s previously reported, known QTL for GLS resistance being used for breeding purposes through application of methods described in Kerns.
Response to Arguments
Applicant urges that obviousness rejection under U.S.C. 103 is improper because the office has not established a prima facie case of obviousness for claims 1 and 5, and that ‘obvious to try’ does not apply in view of In re O’Farrell [Remarks, p.6 par.5—p.7, par.1].
This is not found persuasive because, as established by KSR Int'l Co. v. Teleflex Inc., 550 U.S. 398, 415-421, 82 USPQ2d 1385, 1395-97 (2007), ‘obvious to try’, when choosing from a finite number of solutions, is sufficient to render an invention obvious. See MPEP 2143.I(E). The rationale is that there had been a finite number identified, predictable potential solutions. Benson clearly provides a finite number of solutions with reasonable expectation of successfully finding a locus associated with GLS resistance, which is the exact same trait they teach. It was known the genetic region further characterized by Applicant harbored a gene or sequences associated with GLS resistance in maize.
Further, Applicant argues that prior art both (a) gives no direction as to which of many possible choices are likely to be successful and (b) gives only general guidance in a new technology or ‘promising field of experimentation’.
This is unconvincing, as with respect to (a), the prior art of Benson provides a direct teaching of the specific genetic region harboring Applicant’s GLS resistance. Benson highlights three prioritized QTL regions, with defined boundaries of the DNA region encompassed. The regions each contain a finite number of gene candidates, which Benson also narrows to a list of candidates, systematically narrowing to a smaller and smaller region of DNA sequence. Of the numerous QTL initially detected by Benson, only three were determined to be important enough to warrant fine mapping, one of those three being qGLS2.09 which was fine mapped from an original QTL size of 13Mb to 4Mb, estimated to contain 290 protein-coding genes, or targets [p.11, par.1]. Applicant’s claimed sequence is within the bounds of those taught by Benson, and arrived at by sequencing the DNA within Benson’s QTL.
At the time of filing it was routine to sequence DNA within defined regions. It was also routine to develop mapping populations providing increased genetic mapping resolution. One would simply require the financial or technical resources to sequence the DNA within this region, as originally disclosed by Benson, and apply basic principles of genetic analysis to uncover causative genes or correlated markers. In this sense, Applicant is merely continuing to the stepwise process of narrowing the target DNA sequence(s) first identified as carrying GLS resistance by Benson.
With respect to (b), Benson is not describing a wholly new or unpredictable field of experimentation, but is rather teaching a specific genetic region, associated with a specific phenotype, that would reasonably be considered to harbor a causative gene or markers able to be linked to the same phenotype now being claimed by Applicant. At the time of filing, genetic mapping using molecular markers, and ‘fine mapping’ of chromosomes using iterative steps of increasing sequencing resolution, was known and routine.
The claimed invention is not, as would be argued by Applicant, a foray into an unknown and unpredictable area of genetic experimentation, but instead is a routine genetic mapping and genome sequencing process well-established within the field of plant breeding and genetics. In addition to being routine, such a process would be further facilitated by already having defined boundaries and prioritized candidate genes and/or sequences, as provided in Benson. Applicant is not claiming a region formerly unknown and with no relation to GLS resistance – they are simply providing a more granular description of a QTL region known to confer GLS resistance, taught by Benson. While this informative and valuable to the research community, it is not inventive.
For these reasons, Applicant’s claims clearly represent a routine process whereby plant geneticists provide molecular characterization of an increasingly narrow region associated with a gene through increased use of mapping resources. They do so within previously taught QTL region for the same trait as taught by prior art, albeit using more granular resolution. While this is useful information to plant breeders, it is both predictable and obvious.
Conclusion
No claims are allowed.
THIS ACTION IS MADE FINAL. 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.
Contact Information
Any inquiry concerning this communication or earlier communications from the examiner should be directed to KEITH R WILLIAMS whose telephone number is (571)272-3911. The examiner can normally be reached Mon - Fri, 9:30 - 5:30 EST.
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/KEITH R. WILLIAMS/Examiner, Art Unit 1663
/Anne Kubelik/Primary Examiner, Art Unit 1663
1 See Bubeck et al. Quantitative Trait Loci Controlling Resistance to Gray Leaf Spot in Maize. Crop Sci. 33:838-847 (1993). 838-847