DETAILED ACTION
Applicant's submission filed on December 4, 2025 has been entered.
Claims 2, 6 and 12 are cancelled.
Claim 16 is new.
Claims 3-5, 7-11 and 13-15 are withdrawn.
Claims 1, 3-5, 7-11 and 13-16 are pending.
The text of those sections of Title 35, U.S. Code not included in this action can be found in a prior Office action.
All previous objections and rejections not set forth below have been withdrawn.
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 Rejections - 35 USC § 112
The following is a quotation of the first paragraph of 35 U.S.C. 112(a):
(a) IN GENERAL.—The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor or joint inventor of carrying out the invention.
The following is a quotation of the first paragraph of pre-AIA 35 U.S.C. 112:
The specification shall contain a written description of the invention, and of the manner and process of making and using it, in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and use the same, and shall set forth the best mode contemplated by the inventor of carrying out his invention.
Claims 1 and 16 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the written description requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to reasonably convey to one skilled in the relevant art that the inventor or a joint inventor, or for applications subject to pre-AIA 35 U.S.C. 112, the inventor(s), at the time the application was filed, had possession of the claimed invention.
Claim 1 is drawn to a wheat plant cell having a modified genome that results in the wheat plant cell exhibiting altered vesicular trafficking in comparison to an unmodified wheat plant cell having a reference genome, wherein the modified genome differs from the reference genome by comprising at least one predetermined modification of a gene of interest, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome.
New claim 16 is drawn to the wheat plant cell of claim 1, wherein the gene of interest encodes a protein having at least 98% sequence identity to SEQ ID NO: 848.
The specification at page 188 paragraph [0372] indicates that Table 10 provides a selection of common wheat (Triticum aestivum) genes identified by gene name (taken from a monocot ortholog), gene ID, and sequence identifier (SEQ ID NO:), grouped according to a phenotype or trait expected in a wheat plant in which one or more of these genes is modified in comparison to an unmodified wheat plant having a reference genome. The specification at page 194 in Table 10 indicates that the architectural trait of vesicular trafficking is the phenotype or trait expected to be altered in a wheat plant in which the expression of the gene encoding SEQ ID NO: 848 (ric2) is increased.
The specification indicates that SEQ ID NO: 231 is a monocot orthologue of the Arabidopsis thaliana enhancer OCS obtained from Zea mays that is auxin-responsive, constitutive and able to upregulate the expression of an operably linked gene of interest (Table 8 page 158; Example 20 at pages 216-218 paragraphs [0390]-[0394]).
The specification does not describe or characterize the function of SEQ ID NO: 848 (ric2). The specification also does not describe or characterize the phenotype, i.e. the manner in which vesicular trafficking is altered, of any wheat plant cell or seed or progeny thereof that has a modified genome that differs from a reference genome by comprising at least one predetermined modification of a gene of interest, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome.
With respect to the state of the art regarding the predictability of identifying orthologues, it was known at the time of filing that methods for the prediction of orthologues may fail to correctly identify orthologues due to a variety of different factors that include gene duplication, domain shuffling, speciation and database errors. See, for example, Sjolander (Phylogenomic inference of protein molecular function: advances and challenges. Bioinformatics. 2004 Jan 22;20(2):170-9).
With respect to the state of the art regarding the ability to predict the function of an encoded polypeptide, it was known at the time of filing that the function of an encoded polypeptide cannot reliably be predicted on the basis of its structure alone or its homology to other known proteins, since structurally similar polypeptides may not have the same function.
See, for example, Whisstock J.C. et al. (Prediction of protein function from protein sequence and structure. Q Rev Biophys. 2003 Aug;36(3):307-40. Review), who teach
“... prediction of protein function from sequence and structure is a difficult problem, because homologous proteins often have different functions. Many methods of function prediction rely on identifying similarity in sequence and/or structure between a protein of unknown function and one or more well-understood proteins. Alternative methods include inferring conservation patterns in members of a functionally uncharacterized family for which many sequences and structures are known. However, these inferences are tenuous. Such methods provide reasonable guesses at function, but are far from foolproof.” (Abstract)
Whisstock J.C. et al. also teach at page 309 that while the observation that similar sequences determine similar structures gives us general confidence in homology modeling, much less reliable is the widely held assumption that proteins with very similar sequences should by virtue of their very similar structures have similar functions. Whisstock J.C. et al. further teach at page 309 that to reason from sequence and structure to function is to step on much shakier ground, that while many families of proteins contain homologues with the same function, the assumption that homologues share function is less and less safe as the sequences progressively diverge, and that even closely related proteins can change function through divergence to a related function or by recruitment for as very different function in such cases the assignment of function on the basis of homology in the absence of direct experimental evidence will give the wrong answer.
Whisstock J.C. et al. additionally teach at page 310 that a protein need not even change sequence to change function, as numerous proteins exhibit multiple functions in different cellular environments such that even if detailed in vitro studies on isolated proteins do identity a function we cannot be sure we know the molecules full repertoire of biological activities, and that nonhomologous proteins may conversely have similar functions.
Whisstock J.C. et al. further teach that while general hints based on protein sequence, structure, genomics and interaction patterns may be useful in guiding experimental investigations of protein function,
“inferring protein function from knowledge of the function of a close homologue is like solving the clue of an American crossword puzzle. Finding the word that satisfies the definition may be difficult but the task in principle is straightforward. Working out the function of a protein from its sequence and structure is like solving the clue of a British crossword puzzle. It is by no means obvious which features of the definition are providing the real clues, as opposed to misleading ones. Also, for both types of puzzle and for the suggestion of a protein function, even if your answer appears to fit it may be wrong.” (pages 311-312).
With respect to the state of the art regarding vesicular trafficking in plant cells, it was known at the time of filing that vesicular trafficking in plant cells is a complex process involving a multitude of different cellular compartments and different regulatory pathways.
See, for example, Hawes et al. (Endomembranes and vesicle trafficking. Curr. Opin. Plant Biol. 1999 Dec;2(6):454-61), who teach that analyses of the data accumulated on the structural and functional organization of the endomembrane system and vesicular trafficking in higher plants indicate that it is complex (abstract). Hawes et al. also teach that membrane trafficking between the endoplasmic reticulum, the golgi apparatus, the vacuole and the plasma membrane can follow a number of different routes and use different transport vesicles (page 454; page 455 Figure 1). Hawes et al. additionally teach that the cytoskeleton, lipid metabolism and intracellular signaling are among the components implicated in the regulation of vesicular trafficking in higher plants (pages 458-459).
Given the breadth of the claims which allow for a wheat plant cell having a modified genome that results in the wheat plant cell exhibiting altered vesicular trafficking in comparison to an unmodified wheat plant cell having a reference genome, wherein the modified genome differs from the reference genome by comprising at least one predetermined modification of a gene of interest, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome, given that methods for the prediction of orthologues may fail to correctly identify orthologues, given that the function of an encoded polypeptide cannot reliably be predicted on the basis of its structure alone or its homology to other known proteins, given that vesicular trafficking in plant cells is known to be a complex process involving a multitude of different cellular compartments and regulatory pathways, given the extremely limited disclosure of a single functionally uncharacterized ric2 gene so named based on a monocot ortholog thereof wherein increased expression of the gene is predicted to alter the architectural trait of vesicular trafficking when its expression is increased, and given the absence of any description of the phenotype, i.e. the manner in which vesicular trafficking is altered, of any wheat plant cell comprising any predetermined modification of any ric2 gene, one skilled in the art would not recognize that the applicant was in possession of the claimed invention as a whole at the time of filing.
Response to Arguments
Applicant's arguments filed December 4, 2025 have been fully considered but they are not persuasive.
Applicant traverses the rejection, and maintains that a person of ordinary skill in the art examining the amino acid sequence of SEQ ID NO: 848 would readily recognize that the wheat protein is a member of the Ras superfamily of small GTPases, and more specifically a Rab family small GTPase. Applicant points out that all small GTPases share a conserved G-domain, but the different families (Rab, Rop, Arf, and Ran) are distinguished by characteristic C-terminal or N-terminal motifs and post-translational modifications. Applicant also points out that Rab and Rop GTPases undergo post-translational lipid modification at their C-termini, Arf GTPases are
myristoylated near the N-terminus, and Ran GTPases have a conserved acidic domain (DDDDD/E) at their C-terminus. Applicant additionally points out that Rab GTPases terminate in a CC, CXC, CCX, CCXX, or CCXXX motif, whereas Rop GTPases terminate in a CaaX motif or GC-box.
With respect to the rejected claims, Applicant notes that SEQ ID NO: 848 terminates in a CCXX motif, which is a hallmark of a Rab GTPase. Applicant maintains that Rab GTPases are widely recognized as key regulators of intracellular vesicular transport and trafficking of proteins between organelles of the endocytic and secretory pathways, facilitating vesicle formation and budding from the donor compartment, transport to the acceptor compartment, and subsequent vesicle fusion and release of vesicle contents into the acceptor compartment. Applicant notes that the role of Rab GTPases in vesicle trafficking in plants has been reviewed in, for example, Nielsen, and that, as acknowledged in the Office Action, the specification at page 194 in Table 10 indicates that vesicular trafficking is expected to be altered in a wheat plant when expression of the gene encoding SEQ ID NO: 848 is increased. Applicant maintains that, in view of the conserved Rab GTPase structure of SEQ ID NO: 848, the well-established role of such Rab GTPases in vesicular trafficking, and the explicit assignment of vesicular trafficking to the wheat gene encoding SEQ ID NO: 848 in the originally filed specification, a person of ordinary skill in the art would reasonably conclude that Applicant had possession of the claimed invention at the time the application was filed.
Applicant's arguments are not persuasive.
With respect to Applicant’s assertion that the claimed invention is described because SEQ ID NO: 848 encodes a protein that comprises structural motifs characteristic of an art recognized class of proteins (a Rab family small GTPase of the Ras superfamily of small GTPases), this not persuasive because the presence structural motifs characteristic of Rab GTPases alone is not sufficient to describe the claimed wheat plant cell, since different types of Rab GTPases are known to regulate diverse aspects of plant vesicular trafficking - see, e.g. Nielsen et al. The regulatory RAB and ARF GTPases for vesicular trafficking. Plant Physiol. 2008 Aug;147(4):1516-26, submitted with the IDS filed December 4, 2025.
With respect to Applicant’s assertion that the claimed invention is described because SEQ ID NO: 848 encodes a Rab GTPase, Rab GTPases being known in the art as key regulators of vesicular trafficking, this is not persuasive, because it has not been established that SEQ ID NO: 848 encodes a functional Rab GTPase, and because different types of Rab GTPases are known to regulate diverse aspects of plant vesicular trafficking. See, e.g. Nielsen et al. The regulatory RAB and ARF GTPases for vesicular trafficking. Plant Physiol. 2008 Aug;147(4):1516-26, submitted with the IDS filed December 4, 2025.
The Examiner therefore maintains that the specification does not describe the claimed invention in sufficient detail that one skilled in the art could reasonably conclude that the Applicant had possession of the claimed invention at the time the application was filed. Accordingly, the rejection is maintained.
Claims 1 and 16 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, as failing to comply with the enablement requirement. The claim(s) contains subject matter which was not described in the specification in such a way as to enable one skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention.
Claim 1 is drawn to a wheat plant cell having a modified genome that results in the wheat plant cell exhibiting altered vesicular trafficking in comparison to an unmodified wheat plant cell having a reference genome, wherein the modified genome differs from the reference genome by comprising at least one predetermined modification of a gene of interest, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome.
New claim 16 is drawn to the wheat plant cell of claim 1, wherein the gene of interest encodes a protein having at least 98% sequence identity to SEQ ID NO: 848.
The specification at page 188 paragraph [0372] indicates that Table 10 provides a selection of common wheat (Triticum aestivum) genes identified by gene name (taken from a monocot ortholog), gene ID, and sequence identifier (SEQ ID NO:), grouped according to a phenotype or trait expected in a wheat plant in which one or more of these genes is modified in comparison to an unmodified wheat plant having a reference genome. The specification at page 194 in Table 10 indicates that the architectural trait of vesicular trafficking is the phenotype or trait expected to be altered in a wheat plant in which the expression of the gene encoding SEQ ID NO: 848 (ric2) is increased.
The specification indicates that SEQ ID NO: 231 is a monocot orthologue of the Arabidopsis thaliana enhancer OCS obtained from Zea mays that is auxin-responsive, constitutive and able to upregulate the expression of an operably linked gene of interest (Table 8 page 158; Example 20 at pages 216-218 paragraphs [0390]-[0394]).
The specification does not disclose or characterize the function of SEQ ID NO: 848 (ric2). The specification also does not disclose or characterize the phenotype , i.e. the manner in which vesicular trafficking is altered, of any wheat plant cell or seed or progeny thereof that has a modified genome that differs from a reference genome by comprising at least one predetermined modification of a ric2 gene, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome.
The claimed invention is not enabled because methods for the prediction of orthologues may fail to correctly identify orthologues and paralogues due to a variety of different factors that include gene duplication, domain shuffling, speciation and database errors.
See, for example, Sjolander (Phylogenomic inference of protein molecular function: advances and challenges. Bioinformatics. 2004 Jan 22;20(2):170-9).
The claimed invention is also not enabled because the function of an encoded polypeptide cannot reliably be predicted on the basis of its structure alone or its homology to other known proteins, since structurally similar polypeptides may not have the same function.
See, for example, Whisstock J.C. et al. (Prediction of protein function from protein sequence and structure. Q Rev Biophys. 2003 Aug;36(3):307-40. Review), who teach
“... prediction of protein function from sequence and structure is a difficult problem, because homologous proteins often have different functions. Many methods of function prediction rely on identifying similarity in sequence and/or structure between a protein of unknown function and one or more well-understood proteins. Alternative methods include inferring conservation patterns in members of a functionally uncharacterized family for which many sequences and structures are known. However, these inferences are tenuous. Such methods provide reasonable guesses at function, but are far from foolproof.” (Abstract)
Whisstock J.C. et al. also teach at page 309 that while the observation that similar sequences determine similar structures gives us general confidence in homology modeling, much less reliable is the widely held assumption that proteins with very similar sequences should by virtue of their very similar structures have similar functions. Whisstock J.C. et al. further teach at page 309 that to reason from sequence and structure to function is to step on much shakier ground, that while many families of proteins contain homologues with the same function, the assumption that homologues share function is less and less safe as the sequences progressively diverge, and that even closely related proteins can change function through divergence to a related function or by recruitment for as very different function in such cases the assignment of function on the basis of homology in the absence of direct experimental evidence will give the wrong answer.
Whisstock J.C. et al. additionally teach at page 310 that a protein need not even change sequence to change function, as numerous proteins exhibit multiple functions in different cellular environments such that even if detailed in vitro studies on isolated proteins do identity a function we cannot be sure we know the molecules full repertoire of biological activities, and that nonhomologous proteins may conversely have similar functions.
Whisstock J.C. et al. further teach that while general hints based on protein sequence, structure, genomics and interaction patterns may be useful in guiding experimental investigations of protein function,
“inferring protein function from knowledge of the function of a close homologue is like solving the clue of an American crossword puzzle. Finding the word that satisfies the definition may be difficult but the task in principle is straightforward. Working out the function of a protein from its sequence and structure is like solving the clue of a British crossword puzzle. It is by no means obvious which features of the definition are providing the real clues, as opposed to misleading ones. Also, for both types of puzzle and for the suggestion of a protein function, even if your answer appears to fit it may be wrong.” (pages 311-312).
The claimed invention is additionally not enabled because the manner in which vesicular trafficking is altered cannot reliably be predicted on the basis of increasing the expression of a single gene because vesicular trafficking in plant cells is known to be a complex process involving a multitude of different cellular compartments and different regulatory pathways.
See, for example, Hawes et al. (Endomembranes and vesicle trafficking. Curr. Opin. Plant Biol. 1999 Dec;2(6):454-61), who teach that analyses of the data accumulated on the structural and functional organization of the endomembrane system and vesicular trafficking in higher plants indicate that it is complex (abstract). Hawes et al. also teach that membrane trafficking between the endoplasmic reticulum, the golgi apparatus, the vacuole and the plasma membrane can follow a number of different routes and use different transport vesicles (page 454; page 455 Figure 1). Hawes et al. additionally teach that the cytoskeleton, lipid metabolism and intracellular signaling are among the components implicated in the regulation of vesicular trafficking in higher plants (pages 458-459).
In the instant case the specification does not provide sufficient guidance with respect to how to use a wheat plant cell having a modified genome wherein the modified genome differs from the reference genome by comprising at least one predetermined modification of a gene of interest, wherein the at least one predetermined modification comprises heterologous integration of a nucleic acid sequence that is encoded by at least one donor polynucleotide molecule and that comprises a regulatory element, at a predetermined locus between 1-1000 nucleotides upstream of the start codon of the coding sequence of the gene of interest in the reference genome, wherein the regulatory element comprises SEQ ID NO:231, wherein the gene of interest has at least 95% sequence identity to SEQ ID NO: 1132 or encodes a protein having at least 95% sequence identity to SEQ ID NO: 848, and wherein the predetermined modification results in increased expression of the gene of interest relative to expression of the gene in the reference genome.
Such guidance is necessary because methods for the prediction of orthologues may fail to correctly identify orthologues and paralogues, because the function of an encoded polypeptide cannot reliably be predicted on the basis of its structure alone or its homology to other known proteins, and because the manner in which vesicular trafficking is altered cannot reliably be predicted on the basis of increasing the expression of a single gene. Absent guidance one skilled in the art would have to determine the effect, if any, of a regulatory element that comprises SEQ ID NO: 231 on a variety of aspects of vesicular trafficking when integrated at a predetermined locus between 1 - 1000 nucleotides upstream of the start codon of the coding sequence of a ric2 gene in a wheat plant cell in order to determine which aspect of vesicular trafficking, if any, can be altered. Such a trial and error approach to practicing the claimed invention would constitute undue experimentation
Response to Arguments
Applicant's arguments filed December 4, 2025 have been fully considered but they are not persuasive.
Applicant traverses the rejection, and maintains that the claims also comply with the enablement requirement for at least the reasons discussed above in response to the written description rejection. Applicant maintains that the he specification teaches one skilled in the
art how to make and use the claimed wheat plant cells without undue experimentation. Applicant points, in particular, to Example 20 at paragraphs [0390]-[0394] of the originally filed specification, which provides enabling guidance for producing wheat plant cells comprising the heterologous regulatory element of SEQ ID NO: 231 to increase gene expression that can readily be adapted to the gene encoding SEQ ID NO: 848 as claimed.
Applicant points out that, as discussed above, SEQ ID NO: 848 encodes a Rab GTPase, and Rab GTPases are known in the art as key regulators of vesicular trafficking. Applicant maintains that once one skilled in the art has produced wheat plant cells in which this Rab GTPase is upregulated using the heterologous regulatory element of SEQ ID NO: 231, standard and well-established methods for assessing vesicle formation, transport, and fusion in plant cells (e.g., fluorescence confocal microscopy) could readily be used to determine the nature and extent of the alteration of vesicular trafficking without undue experimentation.
Applicant's arguments are not persuasive.
With respect to Applicant’s assertion that Example 20 provides enabling guidance for producing wheat plant cells comprising the heterologous regulatory element of SEQ ID NO: 231 to increase gene expression that can readily be adapted to the gene encoding SEQ ID NO: 848 as claimed, this is not persuasive, because Example 20 provides no guidance with respect to how to use such a wheat plant cell. Such guidance is necessary because methods for the prediction of orthologues may fail to correctly identify orthologues and paralogues, because the function of an encoded polypeptide cannot reliably be predicted on the basis of its structure alone or its homology to other known proteins, and because the manner in which vesicular trafficking is altered cannot reliably be predicted on the basis of increasing the expression of a single gene. Absent guidance one skilled in the art would have to determine the effect, if any, of a regulatory element that comprises SEQ ID NO: 231 on a variety of aspects of vesicular trafficking when integrated at a predetermined locus between 1 - 1000 nucleotides upstream of the start codon of the coding sequence of a ric2 gene in a wheat plant cell in order to determine which aspect of vesicular trafficking, if any, can be altered. Such a trial and error approach to practicing the claimed invention would constitute undue experimentation.
With respect to Applicant’s assertion that the claimed invention is enabled because SEQ ID NO: 848 encodes a Rab GTPase, Rab GTPases being known in the art as key regulators of vesicular trafficking, this is not persuasive, because it has not been established that SEQ ID NO: 848 encodes a functional Rab GTPase, and because different types of Rab GTPases are known to regulate diverse aspects of plant vesicular trafficking. See, e.g. Nielsen et al. The regulatory RAB and ARF GTPases for vesicular trafficking. Plant Physiol. 2008 Aug;147(4):1516-26, submitted with the IDS filed December 4, 2025.
Absent guidance with respect to whether SEQ ID NO: 848 encodes a functional Rab GTPase, and with respect to which aspects of plant vesicular trafficking are regulated by SEQ ID NO: 848 and how, one skilled in the art would still have to determine the effect, if any, of a regulatory element that comprises SEQ ID NO: 231 on a variety of aspects of vesicular trafficking when integrated at a predetermined locus between 1 - 1000 nucleotides upstream of the start codon of the coding sequence of a ric2 gene in a wheat plant cell in order to determine which aspect of vesicular trafficking, if any, can be altered. Such a trial and error approach to practicing the claimed invention would still constitute undue experimentation, the availability of known techniques for assessing vesicle formation, transport, and fusion in plant cells notwithstanding.
Accordingly, the rejection is maintained.
Conclusion
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.
Remarks
Any inquiry concerning this communication or earlier communications from the examiner should be directed to CYNTHIA E COLLINS whose telephone number is (571)272-0794. The examiner can normally be reached M-F 8:30 am - 5:00 pm.
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/CYNTHIA E COLLINS/Primary Examiner, Art Unit 1662