PERFORMANCE PLANTS, INC.

Patent Trials and Appeals Board

Apr 14, 2021

2020006381 (P.T.A.B. Apr. 14, 2021)

UNITED STATES PATENT AND TRADEMARK OFFICE
UNITED STATES DEPARTMENT OF COMMERCE
United States Patent and Trademark Office
Address: COMMISSIONER FOR PATENTS
P.O. Box 1450
Alexandria, Virginia 22313-1450
www.uspto.gov
APPLICATION NO. FILING DATE FIRST NAMED INVENTOR ATTORNEY DOCKET NO. CONFIRMATION NO.
15/418,412 01/27/2017 Jiangxin Wan PREP-014C01US
322117-2202
3220
58249 7590 04/14/2021
COOLEY LLP
ATTN: IP Docketing Department
1299 Pennsylvania Avenue, NW
Suite 700
Washington, DC 20004
EXAMINER
KUMAR, VINOD
ART UNIT PAPER NUMBER
1663
NOTIFICATION DATE DELIVERY MODE
04/14/2021 ELECTRONIC
Please find below and/or attached an Office communication concerning this application or proceeding.
The time period for reply, if any, is set in the attached communication.
Notice of the Office communication was sent electronically on above-indicated "Notification Date" to the
following e-mail address(es):
zIPPatentDocketingMailboxUS@cooley.com
PTOL-90A (Rev. 04/07)
UNITED STATES PATENT AND TRADEMARK OFFICE
BEFORE THE PATENT TRIAL AND APPEAL BOARD
Ex parte JIANGXIN WAN, YAFAN HUANG, and MONIKA M. KUZMA
Appeal 2020-006381
Application 15/418,412
Technology Center 1600
Before RICHARD M. LEBOVITZ, JOHN G. NEW, and
RACHEL H. TOWNSEND, Administrative Patent Judges.
TOWNSEND, Administrative Patent Judge.
DECISION ON APPEAL
Pursuant to 35 U.S.C. § 134(a), Appellant1 appeals from the
Examiner’s decision to reject claims directed to a method of producing a
heat stress tolerant plant as being obvious. Oral argument was heard April 8,
2021. We have jurisdiction under 35 U.S.C. § 6(b).
We REVERSE.

1 We use the term “Appellant” to refer to “applicant” as defined in 37
C.F.R. § 1.42. Appellant identifies the real party in interest as Performance
Plants, Inc. (Appeal Br. 3.)
Appeal 2020-006381
Application 15/418,412
2
STATEMENT OF THE CASE
Appellant’s Specification states that “[a] number of studies have been
conducted to identify and characterize genes and pathways that are involved
in plant thermotolerance.” (Spec. 2.) Appellant’s invention “relates to a
method for enhancing the heat stress tolerance of plants by means of
increasing the expression” of a protein from the MYB-subgroup 14 family of
transcription factors.2 (Id. at 5.)
Claim 1, reproduced below, is illustrative of the claimed subject
matter:
1. A method of producing a heat stress tolerant plant, comprising:
a) providing a nucleic acid encoding a plant MYB
subgroup-14 polypeptide, wherein said plant MYB subgroup-14
polypeptide is MYB68;
b) inserting said nucleic acid into a vector;
c) transforming a plant, a tissue culture, or a plant cell with
said vector to obtain a transformed plant, tissue culture, or plant
cell;
d) increasing expression of said plant MYB subgroup-14
polypeptide in said transformed plant, tissue culture, or plant cell
as compared to a wild type plant of the same species not
transformed with said vector; and
e) growing said transformed plant or regenerating a plant
from said transformed tissue culture or plant cell, wherein a heat
stress tolerant plant is produced which has an increased heat
stress tolerance as compared to a wild type plant of the same
species not transformed with said vector.

2 “Transcription factors are DNA binding proteins that interact with specific
promoter or enhancer sequences and alter the gene expression of the
associated gene.” (Spec. 2.)
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REFERENCE
The prior art relied upon by the Examiner is:
Name Reference Date
Caiping Feng et al. Arabidopsis MYB68 in
development and
responses to
environmental cues, 167
Plant Sciences 1099–
1107
2004

REJECTION
The following ground of rejection by the Examiner is before us on
review:
Claims 1 and 6 under 35 U.S.C. § 103(a) as being unpatentable over
Feng.
DISCUSSION
Non-Obviousness
The Examiner finds that Feng teaches a method of inserting a nucleic
acid encoding MYB subgroup-14 polypeptide of plant MYB68 into a vector,
and transforming a plant, plant tissue, or plant cell with the vector to obtain a
plant expressing MYB68 protein. (Final Action 3, 6 (citing Feng 1100,
1103).) In particular, the Examiner finds that Feng teaches that an myb68
null mutant plant (which had no detectable MYB68 polypeptide expression)
exhibited a heat sensitive phenotype, but when that mutant was
complemented by expression of wild-type MYB68 protein, the heat sensitive
phenotype was rescued. (Id. at 3; see also id. at 6–7 (referencing Feng 1103
(“the loss of MYB68 function produced by the myb68 mutant phenotype”)).)
The Examiner also finds that Feng teaches that “RT-PCR showed that
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progeny of such transgenic myb68 plants accumulated similar levels of
MYB68 mRNA as wild type (Fig. 2C).” (Id.)
The Examiner notes that Feng does not specifically teach
transforming a wild-type plant with a vector, resulting in overexpression of
the plant MYB68 protein. (Id. at 4.) However, the Examiner concludes that
it would have been obvious to do so “using any strong constitutive or
inducible promoter that were well known in the state of the prior art,
including the one taught by Feng” in light of Feng’s teaching that MYB68
polypeptide functions in heat stress response and tolerance and Feng teaches
it is possible to transform a plant that was a null mutant with such a
polypeptide and achieve a functional result. (Id.) The Examiner concludes
that one of ordinary skill in the art in so doing this would have arrived at the
claimed invention “with a reasonable expectation of success and without any
surprising results.” (Id.) According to the Examiner, the transformed plant
would “[o]bviously” have “exhibited increased expression of MYB68
protein” as compared to wild type and would have resulted in a plant having
heat stress tolerant phenotype. (Id.)
In support of the foregoing, the Examiner notes that McCarthy3
teaches that it was known in the art at the time the invention was made that
CaMV35S can be used as a promoter to overexpress functional orthologs of
Arabidopsis MYB46 and MYB83 transcription factor proteins in a wild-type
Arabidopsis and that such a transformation resulted in elevated expression of
the gene inserted. (Final Action 10–11; Ans. 8.) The Examiner states that
MYB68 has high structural similarity to MYB46 and MYB83. (Id. at 11.)

3 Ryan L. McCarthy, The Poplar MYB Transcription Factors, PtrMYB3 and
PtrMYB20, are Involved in the Regulation of Secondary Wall Biosynthesis,
51(6) Plant Cell Physiology 1084–1090 (2010).
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The Examiner notes that the promoter used in the vector in Feng was not
CaMV35S but rather included a 662 bp heat inducible promoter 5ʹ to the
MYB68 start codon. (Final Action 6.) The Examiner states
Given Feng et al. clearly establishes the function of MYB68
transcription factor protein as a positive regulator of heat stress
tolerance, it would have been obvious and within the scope of
an ordinary skill in the art to have obviously tried to
overexpress MYB68 protein in any plant using any strong stress
(heat) inducible promoter or a constitutive promoter (e.g.
CaMV 35S) that were known and well characterized in the state
of the prior art at the time instant invention was claimed, for the
purpose of producing heat stress tolerant transgenic plants with
a reasonable expectation of success and without any surprising
or unexpected results.
(Id. at 15.) The Examiner further finds that the prior art supports a
reasonable expectation of success that once the gene function is established
through complementation studies, even in diverse organisms including the
yeast and transgenic plant environment, overexpression of said gene in a
transgenic plant environment can produce expected results. (Final Action
11–13 (citing Song,4 Wu,5 and Jako6).) The Examiner argues that Appellant
“has failed to produce any experimental evidence(s) on ‘unpredictable
and/or unexpected results.’” (Id. at 10.)
We disagree with the Examiner’s findings and conclusion of
obviousness.

4 Won-Yong Song et al., Engineering tolerance and accumulation of lead
and cadmium in transgenic plants, 21 Nature Biotechnology 914–19 (2003).
5 Chang-Ai Wu et al., The Cotton GhNHX1 Gene Encoding a Novel
Putative Tonoplast Na+/H+ Antiporter Plays an Important Role in Salt
Stress, 45 Plant Cell Physiol. 600–07 (2004).
6 Coletto Jako et al., Seed-Specific Over-Expression of an Arabidopsis
cDNA Encoding a Diacylglycerol Acyltransferase Enhances Seed Oil
Content and Seed Weight, 126 Plant Physiology 861–74 (2001).
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Appellant concedes that Feng teaches that “growth of the myb68 plant
(resulting from the loss of MYB68 expression), measured as average plant
leaf area, is significantly reduced under hot greenhouse conditions compared
to the wild type plant.” (Appeal Br. 10.) Appellant also concedes Feng
teaches that introduction of a 2012 bp fragment containing the wild type
MYB68 gene results in the myb68 phenotype being complemented to wild
type phenotype. (Id.) Appellant argues, however, that because Feng only
concludes from their data that MYB68 is involved in some steps in root
development that Feng does not teach or suggest this gene provides heat
stress tolerance. (Id. at 10–11.) We do not find this argument persuasive.
Regardless of whether Feng states that MYB68 is involved in heat tolerance,
the data and discussion in Feng at 1103 specifically states that the myb68
phenotype growth “measured as average plant leaf area was significantly
reduced under hot greenhouse conditions compared to wild type (Fig. 2A),”
which “could be complemented to wild type by the introduction” of the
vector producing the wild type MYB68 gene, meaning that “9 of 11
hygromycin resistant lines examined showed no significant growth reduction
at higher temperatures compared to wild type” (emphasis added), implicates
a role for MYB68 in heat stress tolerance. (See also Feng 1106 (“[L]oss of
MYB68 reduces the ability of myb68 plants to compensate their growth at
higher temperatures.”).)
However, we agree with Appellant that the evidence of record
establishes that one of ordinary skill in the art would not have reasonably
expected that overexpression of MYB68 beyond wild type could have been
achieved, and if it had been, would have resulted in “increased heat stress
tolerance as compared to a wild type plant of the same species not
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transformed.” We find the expert testimony of Dr. McCourt7 to establish the
foregoing. First, Feng does not teach achieving overexpression of MYB68
compared to the wild-type plant through complementation of the myb68 null
mutant plant. (McCourt Declaration ¶ 6.) In particular, Dr. McCourt
explains, that contrary to the Examiner’s finding, Feng teaches using the
strong constitutive promoter CaMV 35S in the complementation of myb68
plants and that such transgenic plants have similar levels of MYB68 mRNA
as wild-type. (Id.) Although Dr. McCourt does not explain where Feng
teaches the use of CaMV 35S, we, nevertheless, agree with Dr. McCourt’s
conclusion that CaMV 35S was used to transform the mutant myb68 plants.
In particular, Feng describes the vector that was introduced into
Agrobacterium tumefaciens to be “pCAMBIA1303” (Feng 1100), which
vector is known in the art to include CaMV 35S.8 Moreover, we agree with
Dr. McCourt that Feng teaches the complementation of mutant myb68 plants
with MYB68 did not result in overexpression of MYB68 compared to wild-
type. In particular, Feng describes that “RT-PCR showed that progeny of
such transgenic myb68 plants accumulated similar levels of MYB68 mRNA
as wild type (FIG. 2C).” (Id. at 1103 (emphasis added).)9

7 Declaration of Dr. Peter McCourt dated February 28, 2019.
8 See, e.g., https://www.abcam.com/pcambia1303-plant-expression-vector-
ab275764.html (stating “Plant selection genes in the pCambia vectors are
driven by a double-enhancer version of the CaMV35S promoter and
terminated by the CaMV35S polyA signal” and showing the general
schematic of pCambia1303 including 35S promoter).
9 Besides the foregoing, Dr. McCourt explains that CaMV 35S is known in
the art as a strong constitutive promoter and it is routine practice to use it to
achieve overexpression of a gene in a plant or plant cell and the fact that
overexpression was not achieved in Feng “strongly suggest that MYB68
could not be overexpressed as compared to the endogenous MYB68
expression level in the wild-type.” (McCourt Declaration ¶¶ 2, 6.)
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In addition, Dr. McCourt explains that while it may be possible to
achieve overexpression of a gene in a mutant plant that had previously been
established to have loss of function phenotype due to disruption of gene
expression, one of ordinary skill in the art would not be able to predict a
priori that such overexpression would result in gain of function compared to
wild-type. (McCourt Declaration ¶¶ 7–12.) In particular, Dr. McCourt
presented a review of a number of prior art articles which demonstrate that
overexpression of a gene in a mutant plant that had previously been
established to have a loss of function phenotype due to disruption of gene
expression had different outcomes, such as recovery of wild-type function,
continued inhibitory function, and improved function compared to wild-
type. (Id.) The Examiner does not dispute those findings of Dr. McCourt.
Instead, the Examiner concludes that the references Dr. McCourt discusses
“do not question the fact that complementation of myb68 null mutant (heat
sensitive) by the expression of wild type MYB68 protein establishes the
function of MYB68 protein in heat stress response or tolerance.” (Ans. 15
(emphasis in original).) We find the Examiner’s statement to be irrelevant to
the point raised by Dr. McCourt; namely, that the Examiner’s assertion that
overexpression of a gene compared to wild-type necessarily results in gain
of function related to the gene compared to wild-type is not factually correct.
Dr. McCourt’s testimony supports Appellant’s argument that one of ordinary
skill in the art would not conclude that overexpression of a gene that has
been previously disrupted and shown to result in loss of phenotype would

Dr. McCourt reviews a number of articles where CaMV 35S was used with
other genes and overexpression compare to wild-type was achieved. (Id. ¶¶
3–5.)

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reasonably be expected to result in a gain of phenotype compared to wild
type. (Appeal Br. 12–13.) To the contrary, as indicated by Dr. McCourt’s
testimony, other outcomes are possible and had actually been observed in
the scientific literature he described.
The Examiner’s reliance on McCarthy does not prove the contrary. In
particular, as even the Examiner’s discussion makes clear, McCarthy
restores the wild type phenotype of different MYB genes that have a
different function than the claimed MYB68. (Final Action 10; Ans. 8–9.)
As Appellant notes, there is no evidence that those genes share similar
function to MYB68 or structure. (Appeal Br. 12.) Moreover, the Examiner
did not even establish that the overexpression of these functionally unrelated
genes to MYB68 resulted in gain of function compared to wild-type. Thus,
that McCarthy obtains overexpression of certain MYB genes does not
establish gain of function of heat tolerance by overexpression of MYB68
would have reasonably been expected by one of ordinary skill in the art.
In light of the foregoing, we find the Examiner’s conclusion that one
of ordinary skill in the art would have been motivated to overexpress the
MYB68 gene in the Feng mutant and would have reasonably expected to
arrive at Appellant’s claimed invention without any surprising results has
been adequately rebutted by the evidence of record. Thus, we do not affirm
the Examiner’s rejection of claims 1 and 6 as being obvious from Feng.
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DECISION SUMMARY
Claim(s)
Rejected
35 U.S.C. § Reference(s)/Basis Affirmed Reversed
1, 6 103 Feng 1, 6

REVERSED