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and the fee set forth in 37 CFR 1.17(e) has been timely paid, the finality of the previous Office action has been withdrawn pursuant to 37 CFR 1.114.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 04/02/2026 has been entered.
Claim Status
Claims 1-2, 11-14, 16, 23, 28, 32, 34, 37, 65, and 71 are pending.
Claims 28, 32, 34, 37, 65, and 71 are withdrawn from examination as part of non-elected inventions.
Claims 1-2, 11-14, 16 and 23 are being examined.
All previous objections and rejections not set forth below are withdrawn in view of the amendments by the Applicant.
Claim Rejections - 35 USC § 103
Claims 1-2, 12-14, 16 and 23 remain rejected under 35 U.S.C. 103 as being unpatentable over Christensen et al. (Structure and expression of a maize phytochrome-encoding gene, 1989, Gene, 85:381-390) in view of Kohichi et al. (US7045680B2), Sheehan et al. (Structure and Expression of Maize Phytochrome Family Homeologs, 2004, Genetics, 167: 1395–1405) and Schmidt et al. (The evolving landscape around genome editing in agriculture, 2020, EMBO Reports, 21:e50680).
Claim 1 is drawn to a corn plant or part thereof comprising at least one mutation in the hinge region of the endogenous PHYA gene wherein the encoded PHYA polypeptide comprises the amino acid sequence of GTLNDASKPAQASG (SEQ ID NO: 80), and wherein the corn plant exhibits a reduced Shade Avoidance Response as compared to a control corn plant. Claim 23 depends from claim 1 and is drawn to the at least one mutation results in a mutated PHYA polypeptide having at least 90% sequence identity to any one of SEQ ID NOs: 93-95.
Christensen et al. teach an endogenous corn PHYA2 gene (GenBank Accession No. AY260865) encoding a PHYA2 polypeptide containing a hinge region consisting of SEQ ID NOs: 79-80, as shown in lighter grey (top two rows) in the sequence alignment below. The corn PHYA2 polypeptide also has more than 90% (99.0%) sequence identity to instant SEQ ID NO: 95, as recited in claim 23. Christensen et al. also teach that phytochrome is synthesized de novo in the Pr form and upon red light mediated conversion to the Pfr form, induces a wide variety of photomorphogenic responses (page 382, left column, para 1, line 3-6).
However, Christensen et al. do not describe at least one mutation in the hinge region in the endogenous PHYA2 gene. It also does not teach any shade avoidance response.
Kohichi et al. describe the hinge region starting from amino acid position 541 to 620 (as highlight in darker grey in the sequence alignment below), connecting photosensory domain with the regulatory domain in the oat (A. sativa) Phychrome A protein (Col. 4, line 61-64; Fig. 1) comprising a serine at position 598. Kohichi et al. also describe a modified PHYA polypeptide by substituting serine-598 (with alanine) or its functional equivalent(s) in oat phytochrome A or other phytochrome As from dicotyledonous or monocotyledonous plants (column 6, line 15-18). The modified oat PHYA (SEQ ID NO: 2) polypeptide possesses similar or even greater physiological activity compared to that of wild type PHYA (SEQ ID NO: 4) polypeptide in reducing or suppressing shade avoidance response (column 6, line 19-22). The modified oat phytochrome A gene with an alanine codon replacing the endogenous serine codon giving rise to S598A mutation, which, when expressed, significantly reduce shade avoidance (abstract). Kohichi et al. describe the serine-598 (S598), located in the hinge region, is the only serine residue that is selectively auto-phosphorylated in the Pfr form in vivo (column 4, line 10-12). Phosphorylation of S598 is important for the phytochrome function (column 6, line 53-54). The plant develops a shade avoidance trait when the S598 is substituted with alanine (A) by site-directed mutagenesis (column 4, line 64-67; column 5, line 1-2).
Sequence alignment of the endogenous corn ZmPHYA1 (GenBank Accession No. AY234826, published in 2004 by Sheehan et al.), ZmPHYA2 (GenBank Accession No. AY260865,as taught by Christensen et al.) and the oat AsPHYA protein (SEQ ID NO: 4, as described by Kohichi et al.) containing an endogenous S598 amino acid (serine residue in the box at the bottom row with darker highlight) in SEQ ID NO: 4 as taught by Kohichi et al., indicates that the S598 in the hinge region is a functional equivalent of the serine reside S600 (as recited in claim 11) in the hinge region of the corn PHYA2 proteins (grey highlighted serine residue in the upper box), as shown below.
ZmPHYA1 MSSLRPAQSSSSSSRTRQSSQARILAQTTLDAELNAEYEESGDSFDYSKLVEAQRSTPPE
ZmPHYA2 MSSSRPAHSSSSSSRTRQSSRARILAQTTLDAELNAEYEESGDSFDYSKLVEAQRSTPPE
AsPHYA --MSSSRPASSSSSRNRQSSQARVLAQTTLDAELNAEYEESGDSFDYSKLVEAQRDGPPV
. :******.****:**:*******************************. **
ZmPHYA1 QQGRSGKVIAYLQHIQRGKLIQPFGCLLALDEKSFRVIAFSENAPEMLTTVSHAVPNVDD
ZmPHYA2 QQGRSGKVIAYLQHIQRGKLIQPFGCLLALDEKSFRVIAFSENAPEMLTTVSHAVPNVDD
AsPHYA QQGRSEKVIAYLQHIQKGKLIQTFGCLLALDEKSFNVIAFSENAPEMLTTVSHAVPSVDD
***** **********:*****.************.********************.***
ZmPHYA1 PPKLGIGTNVRSLFTDPGATALQKALGFADVSLLNPILVQCKTSGKPFYAIVHRATGCLV
ZmPHYA2 PPKLGIGTNVRSLFTDPGATALQKALGFADVSLLNPILVQCKTSGKPFYAIVHRATGCLV
AsPHYA PPRLGIGTNVRSLFSDQGATALHKALGFADVSLLNPILVQCKTSGKPFYAIVHRATGCLV
**:***********:* *****:*************************************
ZmPHYA1 VDFEPVKPTEFPATAAGALQSYKLAAKAISKIQSLPGGSMQALCNTVVKEVFDLTGYDRV
ZmPHYA2 VDFEPVKPTEFPATAAGALQSYKLAAKAISKIQSLPGGSMEALCNTVVKEVFDLTGYDRV
AsPHYA VDFEPVKPTEFPATAAGALQSYKLAAKAISKIQSLPGGSMEVLCNTVVKEVFDLTGYDRV
****************************************:.******************
ZmPHYA1 MAYKFHEDEHGEVFAEITKPGIEPYLGLHYPATDIPQAARFLFMKNKVRMICDCRARSVK
ZmPHYA2 MAYKFHEDEHGEVFAEITKPGIEPYIGLHYPATDIPQAARFLFMKNKVRMICDCRARSVK
AsPHYA MAYKFHEDDHGEVFSEITKPGLEPYLGLHYPATDIPQAARLLFMKNKVRMICDCRARSIK
********:*****:******:***:**************:*****************:*
ZmPHYA1 IIEDEALSIDISLCGSTLRAPHSCHLQYMENMNSIASLVMAVVVNENEDDDEPESEQPPQ
ZmPHYA2 IIEDEALSIDISLCGSTLRAPHSCHLKYMENMNSIASLVMAVVVNENEEDDEPEPEQPPQ
AsPHYA VIEAEALPFDISLCGSALRAPHSCHLQYMENMNSIASLVMAVVVNENEEDDEAESEQPAQ
:** ***.:*******:*********:*********************:***.*.***.*
ZmPHYA1 QQKRKKLWGLIVCHHESPRYVPFPLRYACEFLAQVFAVHVNKEFELEKQIREKSILRMQT
ZmPHYA2 QQKKKRLWGLIVCHHESPRYVPFPLRYACEFLAQVFAVHVNKEFELEKQIREKNILRMQT
AsPHYA QQKKKKLWGLLVCHHESPRYVPFPLRYACEFLAQVFAVHVNREFELEKQLREKNILKMQT
***:*:****:******************************:*******:***.**:***
ZmPHYA1 MLSDMLFKESSPLSIVSGSPNIMDLVKCDGAALLYGDKVWRLQTAPTESQIRDIAFWLSE
ZmPHYA2 MLSDMLFKESSPLSIVSGSPNIMDLVKCDGAALLYGDKVWRLQTAPTESQIRDIAFWLSE
AsPHYA MLSDMLFREASPLTIVSGTPNIMDLVKCDGAALLYGGKVWRLRNAPTESQIHDIAFWLSD
*******:*:***:****:*****************.*****:.*******:*******:
ZmPHYA1 VHGDSTGLSTDSLQDAGYPGAASLGDMICGMAVAKITSKDILFWFRSHTAAEIKWGGAKH
ZmPHYA2 VHGDSTGLSTDSLQDAGYPGAASLGDMICGMAVAKITSKDILFWFRSHTAAEIKWGGAKH
AsPHYA VHRDSTGLSTDSLHDAGYPGAAALGDMICGMAVAKINSKDILFWFRSHTAAEIRWGGAKN
** **********:********:*************.****************:*****:
[AltContent: rect]
ZmPHYA1 DPSDEDDSRRMHPRLSFKAFLEVVKMKSLPWSDYEMDAIHSLQLILRGTLNDALKPAQSS
ZmPHYA2 DPSDKDDNRRMHPRLSFKAFLEVVKTKSLPWSDYEMDAIHSLQLILRGTLNDASKPAQAS
AsPHYA DPSDMDDSRRMHPRLSFKAFLEVVKMKSLPWSDYEMDAIHSLQLILRGTLNDASKPKREA
**** **.***************** *************************** ** : :
ZmPHYA1 GLDNQIGDLKLDGLAELQAVTSEMVRLMETATVPILAVDGNGLVNGWNQKVADLSGLRVD
[AltContent: rect]ZmPHYA2 GLDNQIGDLKLDGLAELQAVTSEMVRLMETATVPILAVDGNGLVNGWNQKVAELSGLRVD
AsPHYA SLDNQIGDLKLDGLAELQAVTSEMVRLMETATVPILAVDGNGLVNGWNQKAAELTGLRVD
.*************************************************.*:*:*****
ZmPHYA1 EAIGRHILTLVEDSSVPIVQRMLYLALQGREEKEVRFELKTHGSKRDDGPVILVVNACAS
ZmPHYA2 EAIGRHILTLVEDSSVSLVQRMLYLALQGREEKEVRFELKTHGSKRDDGPVILVVNACAS
AsPHYA DAIGRHILTLVEDSSVPVVQRMLYLALQGKEEKEVRFEVKTHGPKRDDGPVILVVNACAS
:***************.:***********:********:****.****************
ZmPHYA1 RDMHDHVVGVCFVAQDMTVHKLVMDKFTRVEGDYRAIIHNPNPLIPPIFGADQFGWCSEW
ZmPHYA2 RDLHDHVVGVCFVAQDMTVHKLVMDKFTRVEGDYKAIIHNPNPLIPPIFGADQFGWCSEW
AsPHYA RDLHDHVVGVCFVAQDMTVHKLVMDKFTRVEGDYKAIIHNPNPLIPPIFGADEFGWCSEW
**:*******************************:*****************:*******
ZmPHYA1 NAAMTKLTGWHRDEVIDRMLLGEVFDSSNASCLLKSKDAFVRLCIIINSALAGEEAEKAP
ZmPHYA2 NAAMTKLTGWHRDEVVDKMLLGEVFNSSNASCLLKSKDAFVRLCIVINSALAGEEAEKAS
AsPHYA NAAMTKLTGWNRDEVLDKMLLGEVFDSSNASCPLKNRDAFVSLCVLINSALAGEETEKAP
**********:****:*:*******:****** **.:**** **::*********:***.
ZmPHYA1 IGFFDRDGKYIECLLSVNRKVNADGVVTGVFCFIHVPSDDLQHALHVQQASEQTALRRLK
ZmPHYA2 FGFFDRNEKYVECLLSVNRKVNADGVVTGVFCFIHVPSDDLQHALHVQQASEQTAQRKLK
AsPHYA FGFFDRSGKYIECLLSANRKENEGGLITGVFCFIHVASHELQHALQVQQASEQTSLKRLK
:*****. **:*****.*** * .*::*********.*.:*****:********: ::**
ZmPHYA1 AFSYMRHAIDKPLSGMLYSRETLKGTDLDEEQMRQVRVADNCHRQLNKILADLDQDNITD
ZmPHYA2 AFSYMRHAINKPLSGMLYSRETLKSTGLNEEQMRQVRVGDNCHRQLNKILADLDQDNITD
AsPHYA AFSYMRHAINNPLSGMLYSRKALKNTDLNEEQMKQIHVGDNCHHQINKILADLDQDSITE
*********::*********::**.*.*:****:*::*.****:*:**********.**:
ZmPHYA1 KSSCLDLDMAEFVLQDVVVSAVSQVLIGCQGKGIRVACNLPERSMKQKVYGDGIRLQQIL
ZmPHYA2 KSSCLDLDMAEFVLQDVVVSAVSQVLIGCQAKGIRVACNLPERSMKQKVYGDGIRLQQIV
AsPHYA KSSCLDLEMAEFLLQDVVVAAVSQVLITCQGKGIRISCNLPERFMKQSVYGDGVRLQQIL
*******:****:******:******* **.****::****** ***.*****:*****:
ZmPHYA1 SDFLFVSVKFSPAGGSVDISSKLTKNSIGENLHLIDFELRIKHQGAGVPAEILSQMYGED
ZmPHYA2 SDFLFVSVKFSPAGGSVDISSKLTKNSIGENLHLIDFELRIKHRGAGVPAEILSQMYEED
AsPHYA SDFLFISVKFSPVGGSVEISSKLTKNSIGENLHLIDLELRIKHQGLGVPAELMAQMFEED
*****:******.****:******************:******:* *****:::**: **
ZmPHYA1 NREQSEEGLSLLVSRNLLRLMNGDIRHLREAGMSTFILTAELAAAPSAAGH
ZmPHYA2 NKEQSEEGFSLAVSRNLLRLMNGDIRHLREAGMSTFILTAELAAAPSAVGR
AsPHYA NKEQSEEGLSLLVSRNLLRLMNGDVRHLREAGVSTFIITAELASAPTAMGQ
*:******:** ************:*******:****:*****:**:* *:
Before the effective filing date of the invention, it would have been obvious to an ordinarily skilled artisan to mutate the endogenous serine residue(s) in the hinge region of endogenous corn PHYA2 protein, as taught by Christensen et al., especially the S600 amino acid as it is nearest and the most likely functional equivalent of S598 of AsPHYA. An ordinarily skilled artisan would reasonably expect the same phenotype in any other plants (especially other monocots including oat and corn, besides Zoysiagrass) by mutating equivalent serine residue(s) of the S598 in oat PHYA polypeptide. It would also have been obvious to an ordinarily skilled artisan to edit the endogenous PHYA2 gene using the well-known standard technique of CRISPR-Cas to get in-frame deletion(s) (as recited in claims 12, 14 and 16) mutation(s) that disrupt the structure of the PHYA protein around the serine residue(s), especially the S600, in the hinge region of the corn PHYA protein(s) with a realistic goal to achieve the shade avoidance trait.
Before the effective filing date, one with ordinary skill in the art would have been motivated to mutate the endogenous serine residue(s), especially the S600 amino acid in the hinge region of corn PHYA proteins (PHYA1 and/or PHYA2) encoded by PHYA genes using standard methods like chemical/physical mutagenesis or targeted gene editing (e.g., CRISPR_Cas), with a realistic goal to develop the same shade avoidance trait (as evident in Zoysiagrass) in the genome edited corn plant comprising serine to alanine substitution in the hinge region of the PHYA1 protein. Similarly, the artisan would have been motivated to edit the endogenous PHYA2 gene using the well-known standard technique of CRISPR-Cas to get in-frame deletion(s) (as recited in claims 12, 14, and 16) of the serine residue(s), especially the S600, in the hinge region with a realistic expectation of success to achieve the same shade avoidance trait, as described by Kohichi et al. One with ordinary skill in the art also would know that many countries starting with Australia and now comprising USA and Canada besides others, do not impose regulatory constraints, which are valid for transgenic crops or GMOs, on genome edited crops, as described by Schmidt et al. (Fig. 1). The artisan would have been motivated to edit the endogenous PHYA gene in corn as compared to expressing a transgene comprising the mutated PHYA gene in corn.
Regarding claim 2, phytochrome is a well-known and the best characterized photoreceptor controlling light response and photomorphogenesis in plants (Christensen et al., page 381, right column, para 1), capable of regulating response to illumination in plants including a corn plant.
Regarding claim 13, the PHYA2 polypeptide described by Kohichi et al. comprises four amino acid substitutions (which implies substituting an A, a T, a G or a C) in the hinge region encoding the S600 (to substitute to alanine) of instant SEQ ID NO: 74, as discussed above.
Response to Applicant’s arguments
The argument set forth in the Applicant’s replies on 04/02/2026 has been fully considered.
but is not found persuasive.
The Applicant argues that, “… Applicant respectfully submits that in addition to
failing to teach or suggest mutation in a region of an endogenous PHYA gene encoding a hinge region or that the PHYA polypeptide therein confers shade avoidance response, Christensen also fails to teach, suggest, or provide any guidance whatsoever for introducing any mutation at any location in a PHYA gene.” (p. 3, para 2, line 3-7). The Applicant continues, “… “Kohichi fails to teach or suggest that a hinge region is a structural feature of all PHYA polypeptides, or more specifically a structural feature of a corn PHYA polypeptide” (p. 10, para 2, line 1-2) and “… Kohichi fails to teach or suggest the introduction of at least one mutation in any endogenous PHYA gene. Rather, Kohichi merely describes a transgenic zoysiagrass that constitutively overexpresses an oat phytochrome A polypeptide having a S598A mutation” (p. 9, para 4, line 2-5). The Applicant argues that the “… teachings of Kohichi (i.e., “Although engineering of shade
avoidance by introducing a foreign PHYA gene was successful in dicotyledonous plants (Boylan and Quail, 1989), transgenic rice plants that overexpress a PHYA gene did not show such a dwarfish appearance”) would suggest to one of ordinary skill in the art that overexpression of the PHYA gene in some plants confers a shade avoidance response, while overexpression of the PHYA gene in other plants fails to confer a shade avoidance response” (p. 11, para 2-3)..
The Examiner disagrees. Christensen et al. teaches an endogenous corn PHYA2 gene that comprises a serine residue at position 600, which is interpretated by the Examiner as a functionally equivalent position of 598 of oat PHYA polypeptide, as described above. Hinge region is a well-known and well characterized domain in all plant phytochrome proteins (both type I and type II phytochrome proteins) connecting the N-terminal photosensory and the C-terminal regulatory domains (the bridging paragraph before column 4 and 5 in Kohichi et al.; Zhou et al. Hinge region of Arabidopsis phyA plays an important role in regulating phyA function, 2018, PNAS, 115: E11864–E11873; p. E11864, para 1, last 4 lines). Kohichi et al. describe the shade avoidance trait in the transgenic Zoysiagrass plant (over)expressing a mutated oat PHYA (not the wild type rice or oat PHYA gene) comprising a mutated serine-598 which, Kohichi et al. assert, is also valid for “its (S598) functional equivalent(s) in oat or other phytochrome As from dicot and monocot plants (column 6, line 15-18). In the response, the Applicant, citing Kohichi et al., asserts that “overexpression of the PHYA gene in other plants fails to confer a shade avoidance response”, as mentioned above. Thus, it is obvious that the phenotype that Kohichi et al. observed is not due to overexpression but the mutation in the hinge region.
Zoysiagrass was used as an example, even though Kohichi et al. describes that the method is valid in other plants including crop plants as well (column 4, line 42-46).
The Applicant does not provide any evidence that indigenous/native or “normal” expression of the mutated oat PHYA protein (in position equivalent to S598A) under the control of PHYA native promoter in oat, Zoysiagrass, or any other plant including corn fail(s) to achieve shade avoidance trait. Applicant’s opinion cannot take the place of evidence (MPEP 716.01(c)(II), 2145(I)).
An ordinarily skilled artisan would have been motivated to edit the endogenous PHYA2 gene in corn using the well-known standard technique of CRISPR-Cas (which was developed and applied in plants much later than 2006, publication year of Kohichi et al.) to mutate the endogenous serine residues especially the S600, which is in the hinge region of the PHYA protein, with the realistic expectation of success to achieve the same shade avoidance trait in a commercially important crop, corn. The combined teaching of Christensen et al. and Kohichi et al. make it obvious to an ordinarily skilled artisan to mutate the serine residues mainly the S600 in the hinge region of endogenous PHYA gene in corn.
One with ordinary skill in the art also would also know that many countries including United States that do not consider genome edited plants as transgenic or GMO, and so do not impose regulatory constraints on genome edited plants as compared to transgenic plants and GMOs, as described by Schmidt et al. (Fig. 1). The artisan would have been motivated to edit the endogenous PHYA gene in corn to overcome such regulatory hurdles, which are imposed on GMO and transgenic plants, in many countries.
The Applicant is reminded that substituting the endogenous promoter with a corn constitutive promoter including a corn ubiquitin promoter (Ubi-P), along with the mutation(s) in the coding region (as described above) comprising and/or around the serine reside(s) in the hinge region also satisfies the claim limitation of “…comprising at least one mutation in an endogenous gene encoding a Phytochrome A (PHYA) polypeptide…”. Such a corn plant is also expected to have the shade avoidance trait, as per the teachings of Kohichi et al. The Applicant does not provide any evidence that constitutive expression of the said mutated PHYA gene in corn would not be having the shade avoidance trait. Applicant’s opinion cannot take the place of evidence (MPEP 716.01(c)(II), 2145(I)).
Conclusion
No claim is allowed.
Communication
Any inquiry concerning this communication or earlier communications from the examiner should be directed to JAY CHATTERJEE whose telephone number is (703)756-1329. The examiner can normally be reached (Mon - Fri) 8.30 am to 5.30 pm..
Examiner interviews are available via telephone, in-person, and video conferencing using a USPTO supplied web-based collaboration tool. To schedule an interview, applicant is encouraged to use the USPTO Automated Interview Request (AIR) at http://www.uspto.gov/interviewpractice.
If attempts to reach the examiner by telephone are unsuccessful, the examiner’s supervisor, Bratislav Stankovic can be reached at (571) 270-0305. The fax phone number for the organization where this application or proceeding is assigned is 571-273-8300.
Information regarding the status of published or unpublished applications may be obtained from Patent Center. Unpublished application information in Patent Center is available to registered users. To file and manage patent submissions in Patent Center, visit: https://patentcenter.uspto.gov. Visit https://www.uspto.gov/patents/apply/patent-center for more information about Patent Center and https://www.uspto.gov/patents/docx for information about filing in DOCX format. For additional questions, contact the Electronic Business Center (EBC) at 866-217-9197 (toll-free). If you would like assistance from a USPTO Customer Service Representative, call 800-786-9199 (IN USA OR CANADA) or 571-272-1000.
Jay Chatterjee
Patent Examiner
Art Unit 1662
/Jay Chatterjee/Examiner, Art Unit 1662
/BRATISLAV STANKOVIC/Supervisory Patent Examiner, Art Units 1661 & 1662
Prosecution Insights