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 .
Continued Examination Under 37 CFR 1.114
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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 6/30/2026 has been entered.
Respond to Amendment
The request for continued examination and accompanying amendment filed on June 30, 2026, have been entered and considered. Claims 1, 5, and 7 are pending. The claims presently under examination are the same as those examined in the prior Final Office Action. Accordingly, the prior rejections have been reconsidered in view of the RCE submission and are maintained, modified, or newly made as set forth below.
Claim Status
Claims 1, 5 and 7 are pending.
Claims 1, 5 and 7 are examined on the merits.
Claim Rejections - 35 USC § 112
The following is a quotation of 35 U.S.C. 112(b):
(b) CONCLUSION.—The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the inventor or a joint inventor regards as the invention.
The following is a quotation of 35 U.S.C. 112 (pre-AIA ), second paragraph:
The specification shall conclude with one or more claims particularly pointing out and distinctly claiming the subject matter which the applicant regards as his invention.
The following rejection is newly made in this Office action.
Claims 1 and 7 rejected under 35 U.S.C. 112(b) or 35 U.S.C. 112 (pre-AIA ), second paragraph, as being indefinite for failing to particularly point out and distinctly claim the subject matter which the inventor or a joint inventor (or for applications subject to pre-AIA 35 U.S.C. 112, the applicant), regards as the invention.
Claim 1, alternative (b), recites down-regulating the gene expression or protein activity of PHR2, but further recites that such down-regulation comprises modifying the promoter region of PHR2 downstream target genes and deleting P1BS elements. Modifying the promoter of a downstream target gene would directly alter expression of the downstream target gene, rather than the gene expression or protein activity of PHR2. Therefore, it is unclear whether the claim requires down-regulation of PHR2 itself or down-regulation of a PHR2 downstream target gene, and the scope of the claim cannot be determined with reasonable certainty.
Claim 7 depends from claim 1 and therefore incorporates all limitations of claim 1. Alternative (b) of claim 1 requires down-regulating PHR2 by modifying the promoter region of PHR2 downstream target genes and deleting P1BS elements. Claim 7, however, further requires that PHR2 exert its regulating function on the downstream target genes by binding to the P1BS element.
It is unclear how PHR2 can exert its regulating function by binding to a P1BS element that has been deleted pursuant to alternative (b) of claim 1. Consequently, one of ordinary skill in the art would not be reasonably apprised whether claim 7 encompassed only the up-regulation embodiment of claim 1, encompasses the down-regulation embodiment despite deletion of the P1BS element, or requires the presence and deletion of different P1BS elements. The scope of claim 7 is therefore unclear.
The following is a quotation of 35 U.S.C. 112(d):
(d) REFERENCE IN DEPENDENT FORMS.—Subject to subsection (e), a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following is a quotation of pre-AIA 35 U.S.C. 112, fourth paragraph:
Subject to the following paragraph [i.e., the fifth paragraph of pre-AIA 35 U.S.C. 112], a claim in dependent form shall contain a reference to a claim previously set forth and then specify a further limitation of the subject matter claimed. A claim in dependent form shall be construed to incorporate by reference all the limitations of the claim to which it refers.
The following rejection is newly made in this Office action.
Claim 7 rejected under 35 U.S.C. 112(d) or pre-AIA 35 U.S.C. 112, 4th paragraph, as being of improper dependent form for failing to further limit the subject matter of the claim upon which it depends, or for failing to include all the limitations of the claim upon which it depends.
Claim 7 depends from claim 1 and therefore incorporates all limitations of claim 1. Alternative (b) of claim 1 requires deleting the P1BS element from the promoter region of a PHR2 downstream target gene by binding to the P1BS element, which requires that the P1BS element remain present. Thus, claim 7 is inconsistent with, rather than a further limitation of, alternative (b) of claim 1.
Applicant may cancel the claim(s), amend the claim(s) to place the claim(s) in proper dependent form, rewrite the claim(s) in independent form, or present a sufficient showing that the dependent claim(s) complies with the statutory requirements.
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.
The following rejection is newly made in this Office action.
Scope of Enablement
Claims 1 and 7 are rejected under 35 U.S.C. 112(a) or 35 U.S.C. 112 (pre-AIA ), first paragraph, because the specifications, while being enabling deletion of the three specifically identified P1BS elements grom the OsPT11 promoter to reduce OsPT11 expression; does not reasonably provide enablement for the full scope of alternative (b), which requires down-regulating the gene expression or protein activity of PHR2 by modifying the promoter region of a PHR2 downstream target gene and deleting P1BS elements. The specification does not enable any person skilled in the art to which it pertains, or with which it is most nearly connected, to make and/or use the invention commensurate in scope with these claims.
An “analysis of whether a particular claim is supported by the disclosure in an application requires a determination of whether that disclosure, when filed, contained sufficient information regarding the subject matter of the claims as to enable one skilled in the pertinent art to make and use the claimed invention.” MPEP 2164.01. “A conclusion of lack of enablement means that. . . the specification, at the time the application was filed, would not have taught one skilled in the art how to make and/or use the full scope of the claimed invention [i.e. commensurate scope] without undue experimentation.” In re Wright, 999 F.2d 1557,1562, 27 USPQ2d 1510, 1513 (Fed. Cir. 1993); MPEP 2164.01.
In In re Wands, 858 F.2d 731,8 USPQ2d 1400 (Fed. Cir. 1988), several factors implicated in determination of whether a disclosure satisfies the enablement requirement and whether any necessary experimentation is “undue” are identified. These factors include, but are not limited to:
(A) The breadth of the claims;
(B) The nature of the invention;
(C) The state of the prior art;
(D) The level of one of ordinary skill;
(E) The level of predictability in the art;
(F) The amount of direction provided by the inventor;
(G) The existence of working examples; and
(H) The quantity of experimentation needed to make or use the invention based on the content of the disclosure. In re Wands, 858 F.2d 731,737, 8 USPQ2d 1400, 1404 (Fed. Cir. 1988). No single factor is independently determinative of enablement; rather “[i]t is improper to conclude that a disclosure is not enabling based on an analysis of only one of the above factors while ignoring one or more of the others.” MPEP 2164.01. Likewise, all factors may not be relevant to the enablement analysis of any individual claim.
Claim 1, alternative (b), is directed to a method of down-regulating the gene expression or protein activity of PHR2 in gramineous plants by modifying the promoter region of a PHR2 downstream target gene and deleting P1BS elements, thereby inhibiting symbiosis between gramineous plants and arbuscular mycorrhizal fungi. Under its broadest reasonable interpretation, the claim is not limited to any particular promoter sequence, P1BS element, genome-editing techniques, or experimental conditions. Although PT11 is recited as the downstream target gene in claim 1(b), the claim encompasses the full scope of performing this approach in gramineous plants. Claim 7 depends from claim 1 and therefore includes all limitations of claim 1, including alternative (b), while further specifying that PHR2 regulates one or more recited downstream target genes by binding to P1BS elements.
The specification discloses that PHR2 binds P1BS elements located in the promoters of downstream target genes and activates expression of those downstream genes. the specification further demonstrates in Example 8 that deletion of all three P1BS elements from the OsPT11 promoter eliminates OsPT11 promoter-driven reporter expression. Thus, the disclosed P1BS deletion reduces expression of the downstream target gene PT11.
The specification, however, does not disclose or demonstrate that deleting P1BS elements from the PT11 promoter down-regulates the gene expression or protein activity of the upstream transcription factor PHR2 itself. Rather, the disclosed regulatory relationship proceeds in the opposite direction: PHR2 binds the P1BS elements and regulates PT11 expression. Although the specification generally lists modification of a downstream target-gene promoter and reduction of P1BS elements as a method of down-regulating PHR2, it provides no working example, mechanistic explanation, or technical guidance showing how deletion of P1BS elements from the PT11 promoter would decrease PHR2 expression or PHR2 protein activity.
The specification provides insufficient direction and no working example for producing the claimed down-regulation of PHR2 through modification of the PT11 promoter. The nature of transcriptional regulatory and feedback pathways is complex and unpredictable, and the specification dos not identify any feedback mechanism through which reduced PT11 expression would reduce PHR2 expression or activity. The unpredictability is demonstrated by the specification itself. The specification teaches that deletion of the P1BS elements from the PT11 promoter abolishes PT11 promoter activity (Example 8), but does not demonstrate any corresponding reduction in PHR2 gene expression or PHR2 protein activity. Thus, although the downstream target gene is affected, the specification provides no evidence that officiation of a downstream target gene promoter produces the claimed down-regulation of PHR2. A person of ordinary skill in the art would therefore have been required to design and test numerous promoter modifications and evaluated their effects on both PT11 and PHR2 to determine whether any such modification produced the claimed results.
Accordingly, the quantity of experimentation required to practice the full scope of alternative (b) would have been undue. Speechification enables direct down-regulation of PHR2 through knockout, silencing , mutation, or gene editing of PHR2 itself, and it enables down-regulation of PT11 through deletion of P1BS elements from the PT11 protomer, but it does not enable the claimed down-regulation of PHR2 by deleting P1BS elements from the promoter of its downstream target gene PT11.
Claim Rejections - 35 USC § 102
The following is a quotation of the appropriate paragraphs of 35 U.S.C. 102 that form the basis for the rejections under this section made in this Office action:
A person shall be entitled to a patent unless –
(a)(1) the claimed invention was patented, described in a printed publication, or in public use, on sale, or otherwise available to the public before the effective filing date of the claimed invention.
(a)(2) the claimed invention was described in a patent issued under section 151, or in an application for patent published or deemed published under section 122(b), in which the patent or application, as the case may be, names another inventor and was effectively filed before the effective filing date of the claimed invention.
The following rejection is newly made in this Office action.
Claims 1 and 5 are rejected under 35 U.S.C. 102(a)(1) as being anticipated by Zhou (Jie Zhou et. al., Plant Physiology (2008) Volume 146, Issue 4, pp1673–1686).
Claim 1 recites a method for regulating symbiosis between Gramineous plants and arbuscular mycorrhizal fungi, and regulating the inhibitory effect of phosphate on arbuscular mycorrhizal symbiosis, the method comprises: regulating gene expression or protein activity of phosphate starvation response factor PHR2 in Gramineous plants selected from:
a) up-regulating the gene expression or protein activity of phosphate starvation response factor PHR2 in Gramineous plants, thereby promoting the symbiosis of plants and arbuscular mycorrhizal fungi, and antagonizing the inhibitory effect of phosphate on arbuscular mycorrhizal symbiosis, wherein said up-regulating the gene expression or protein activity of phosphate starvation response factor PHR2 comprises transferring the encoding sequence of phosphate starvation response factor PHR2 into the Gramineous plants; wherein the PHR2 is selected from a polypeptide having the amino acid sequence of SEQ ID NO: 2.
Broadest Reasonable Interpretation
Under the broadest reasonable interpretation consistent with the specification, alternative (a) of claim 1 recites a method comprising up-regulating the gene expression or protein activity of phosphate starvation response factor PHR2 by transferring the encoding sequence of PHR2 into a Gramineous plant.
The claim expressly defines the up-regulation step by reciting that “said up-regulating…comprises transferring the encoding sequence of phosphate starvation response factor PHR2 into the Gramineous plants”. Thus, the affirmative method requires transferring the PHR2 coding sequence into the Gramineous plant to up-regulate PHR2 gene expression or protein activity. The remaining language reciting promotion of symbiosis and antagonizing the inhibitory effect of phosphate describes the functional result of the recited up-regulation rather than separate affirmative method steps.
The present rejection is based on embodiment (a) of claim 1; embodiment (b) is not relied upon in this rejection.
Zhou discloses a method of regulating the expression and activity of the phosphate starvation response factor OsPHR2 in rice by transferring an OsPHR2 coding sequence into rice and producing OSPHR2-overexpressing transgenic plants (p1673, Abstract). BLAST analysis establishes that the OsPHR2 protein disclosed by Zhou is 100% identical to SEQ ID NO: 2 of the instant application (see below). Zhou constructs an overexpression vector containing the OSPHR2 open reading frame under the control of the cauliflower mosaic virus 35S promoter and transforms rice to generate transgenic plants exhibiting elevated OsPHR2 expression (p1684, left column, pa3). Zhou confirms increased OsPHR2 transcript expression in the resulting transgenic rice Plants (p1676, Fig 3). Thus, Zhou expressly discloses transferring the encoding sequence of the claimed phosphate starvation response factor PHR2 into a gramineous plant to up-regulate PHR2 gene expression, as recited in alternative (a) of claim 1.
Under the broadest reasonable interpretation, the affirmative method recited in alternative (a) is the transfer of the PHR2 encoding sequence into rice to up-regulate PHR2 expression or activity. Zhou performs the same affirmative method step by introducing the OsPHR2 coding sequence into rice to increase PHR2 expression. The “thereby promoting..” language merely states the biological results or consequence of performing the recited up-regulation method, rather than requiring an additional affirmative step or separate manipulation. Therefore, Zhou anticipates alternative (a) of claim 1.
Claim 5 is drawn to the method of claim 1, wherein the regulation of symbiosis between Gramineous plants and arbuscular mycorrhizal fungi or the regulation of inhibitory effect of phosphate on arbuscular mycorrhizal symbiosis comprises up-regulating gene expression or protein activity of PHR2 under low-phosphate conditions, promoting symbiosis between plants and arbuscular mycorrhizal fungi, and increasing phosphate uptake.
Regarding claim 5, Zhou further discloses evaluating OsPHR2-overexpressing transgenic rice plants under low-phosphate and high-phosphate conditions and reports increased phosphate accumulation in the OsPHR2-overexpression plant under both conditions (p1676, left column, pa3; Fig. 3). Thus, Zhou discloses up-regulating PHR2 under low-phosphate conditions and increasing phosphate acquisition, as recited in claim 5. Consistent with interpretation of claim 1 above, the language concerning promotion of symbiosis describes the biological result of the recited PHR2 up-regulation rather than a separate affirmative method step. Therefore, Zhou anticipates claim 5.
Claim Rejections - 35 USC § 103
The following is a quotation of 35 U.S.C. 103 which forms the basis for all obviousness rejections set forth in this Office action:
A patent for a claimed invention may not be obtained, notwithstanding that the claimed invention is not identically disclosed as set forth in section 102, if the differences between the claimed invention and the prior art are such that the claimed invention as a whole would have been obvious before the effective filing date of the claimed invention to a person having ordinary skill in the art to which the claimed invention pertains. Patentability shall not be negated by the manner in which the invention was made.
The following rejection is modified from the prior Office action to reflect the amended claims and/or the additional findings set forth below.
Claim 7 is rejected under 35 U.S.C. §103 as being unpatentable over Zhou (2008) as apply to claim 1, in view of Yang (Shu-Yi Yang et. all., The Plant Cell (2012), Volume 24, Issue 10, pp4236–4251), and further in view of Wu (Ping Wu et. al., Current Opinion in Plant Biology (2013) Volume 16, Issue 2, pp 205-212).
Claim 1 as the teaching of Zhou is discussed above.
Claim 7 is interpreted as depend of claim 1.
Claim 7 is drawn to the method of claim 1, wherein the PHR2 has a regulating function on downstream target genes, wherein the downstream target genes comprise arbuscular mycorrhizal symbiosis-specific phosphate transporter PT11; wherein the PHR2 exerts the regulating function by binding to the P1BS element of downstream target genes.
Under BRI , claim 7 requires that PHR2 regulate at least one of the recited downstream target genes by binding to a P1BS cis-element associated with the downstream target gene. For purposes of this rejection, the Examiner relies on the PT11 alternative.
Zhou anticipates the method of claim 1 for the reason set forth above, but does not expressly teach that PT11 is an arbuscular mycorrhizal symbiosis-specific downstream target of PHR2 or that PHR2 regulates PT11 through binding to P1BS element.
Wu teaches that PHR2 is a transcription factor that binds to P1BS elements in the promoter of phosphate starvation-induced phosphate transporter genes (OsPTs) and activates their expression (page 206, left column, page 207 table 1). Wu specifically identifies PT11 (OsPT11, in rice) as one of these downstream target genes whose promoter contain P1BS motifs and whose expression is up-regulated by PHR2 (page 206, left column, page 207 table 1). Accordingly, Wu teaches that PHR2 has a regulating function on downstream target genes that comprise PT11, and that this regulating function is exerted by binding to the promoter region of PT11, including P1BS elements (page 206, figure 1, table 1 ), thereby meeting the mechanistic “promoter” and “P1BS element” aspect recited in claim 7.
Yang teaches that PT11 (OsPT11) is a mycorrhiza-associated phosphate transporter required for arbuscular mycorrhizal (AM) symbiotic phosphate uptake in rice. Yang shows that PT11 is specifically involved in AM-dependent phosphate uptake and that disruption of PT11 impairs this symbiotic uptake. Thus, Yang identified PT11 as a mycorrhizal symbiosis-specific phosphate transporter and links PT11 function to the promotion of AM symbiosis-associated phosphate acquisition (page 4239, right column, paragraph 2-3).
It would have been obvious to one of ordinary skill in the art, when carrying out Zhou’s method of up-regulating OsPHR2 in rice, to regulate the downstream PT11 gene through the PHR2-P1BS regulatory mechanism taught by Wu. A skilled artisan would have been motivated to apply that known mechanism because Wu identifies PT11 as a PHR2-regulated phosphate transporter gene, and Yang established that PT11 is specifically involved in AM-symbiotic phosphate uptake.
A person of ordinary skill in the art would have had a reasonable expectation that OsPHR2, when overexpressed in rice as taught by Zhou, would regulate OsPT11 through P1BS elements associated with the PT11 promoter because Wu teaches the conserved PHR2-P1BS regulatory mechanism and identifies OsPT11 as a PHR2-regulated phosphate-transporter gene, while Yang confirms the role of OsPT11 in arbuscular-mycorrhizal-symbiotic phosphate uptake. Accordingly, the combined teachings of Zhou, Wu, and Yang render the additional limitations of claim 7 obvious.
Response to Applicant’s Remarks:
Applicant’s arguments filed June 30, 2026 have been fully considered but are not persuasive for the reason set forth below.
(1)Applicant argues that Zhou does not teach symbiosis between rice and arbuscular mycorrhizal fungi, and that Zhou does not expressly teach that OsPHR2 overexpression promotes arbuscular mycorrhizal symbiosis overcomes phosphate-mediated suppression.
As explained in the anticipation rejection above, the recited promotion of arbuscular mycorrhizal symbiosis and antagonism of phosphate inhibition are functional results of the claimed PHR2 up-regulation and do not require separate affirmative method steps. Accordingly, Zhou anticipate claims 1 and 5 despite not expressly discussing arbuscular mycorrhizal symbiosis.
With respect to claim 7, the rejection is not based on Zhou alone. Wu teaches the PHR2-P1BS-PT11 regulatory relationship, and Yang teaches that PT11 is an arbuscular-mycorrhizal-symbiosis-associated phosphate transporter. Therefore, the combined teachings of Zhou, Wu, and Yang render claim 7 obvious.
(2)Applicant further argues that Zhou’s discussion of OsPT9 is irrelevant because PT9 and PT11 have relatively low sequence identity.
This argument is not persuasive because neither the anticipation rejection of claim 1 and 5 nor the obviousness rejection of claim 7 relies on PT9 and PT11 having the same protein sequence or sharing function based on sequence homology. Zhou is relied upon for teaching OsPHR2 overexpression and activation of phosphate starvation/phosphate transporter pathways in rice. Wu is relied upon for teaching that PT11 is a downstream target associated with the PHR/P1BS regulatory pathway. Yang is relied upon for teaching that PT11 functions in arbuscular mycorrhizal symbiotic phosphate uptake. Therefore, the alleged low sequence identity between PT9 and PT11 does not overcome the anticipation rejection of claims 1 and 5 or the obviousness rejection of claim 7.
(3)Applicant also argues that there is no motivation to combine Zhou with Yang and Wu.
This argument is not persuasive. A person of ordinary skill in the art would have been motivated to combine the references because each reference concerns phosphate acquisition/signaling in rice. Zhou teaches OsPHR2 as an upstream phosphate starvation regulator that increases phosphate accumulation. Wu teaches the mechanistic link between PHR2, P1BS elements, and downstream phosphate transporter genes including PT11. Yang teaches that PT11 is required for arbuscular mycorrhizal symbiotic phosphate uptake and that phosphate levels affect arbuscular mycorrhizal colonization. Thus, one of ordinary skill in the art would have had reason to combine Zhou with Wu to apply the know PHR2/P1BS regulatory mechanism to PT11, with a reasonable expectation of achieving the PT11 regulation through P1BS binding recited in claim 7.
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Conclusion
No claims are allowed.
Any inquiry concerning this communication or earlier communications from the examiner should be directed to YANXIN SHEN whose telephone number is (571)272-7538. The examiner can normally be reached Monday-Friday.
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/YANXIN SHEN/Examiner, Art Unit 1663
/WEIHUA FAN/Primary Examiner, Art Unit 1663
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