Full opinion text
OPINION McKELYIE, District Judge. TABLE OF CONTENTS FACTUAL AND PROCEDURAL BACKGROUND 205 A. The Status of the Case. 205 B. Background Information on Bacillus Thuringiensis 206 C. Background Information on Genetic Engineering... 207 D. Mycogen’s Patents. 209 E. Monsanto’s Patent. 214 F. Claim Construction. 215 G. Jury Trial. 216 H. Jury Verdict . 235 I. Post-Trial Motions. 236 II. DISCUSSION 236 A. What is the Standard for Granting Judgment as a Matter of Law?. 236 B. Should the Court Grant Mycogen’s Motion for JMOL that the Claims of the ’600 and ’862 Patents Are Not Invalid Due to Prior Invention? 237 C. Is Mycogen Entitled to Judgment as a Matter of Law that Defendants’ Accused Genes and Gene Products Infringe the Asserted Claims of the ’600 and ’862 Patents?.242 D. Are the Asserted Claims of the ’600 and ’862 Patents Invalid for Obviousness and Anticipation?. 251 E. Are the Claims of the ’600 and ’862 Patents Invalid for Failure to Satisfy the Best Mode Requirement?. 252 F. Are the Claims of the ’600 and ’862 Patents Invalid Due to Indefiniteness? . 254 G. Are the Claims of the ’600 and ’862 Patents Invalid for Lack of Enablement?. 257 H. Should the Court Grant Mycogen’s Motion for a New Jury Trial?. 260 I. Should the Court Grant Defendants’ Motion for Attorneys’ Fees? . 269 J. Should the Court Grant Defendants’ Motion to Amend Judgment?. 272 III. CONCLUSION 273 This is a patent case. Plaintiff Mycogen Plant Science, Inc. owns U.S. Patent No. 5,567,600 (“the ’600 patent”) and U.S. Patent No. 5,567,862 (“the ’862 patent”) which are directed to a synthetic gene inserted into plants to make plants insect-resistant. Michael J. Adang, Elizabeth E. Murray, Thomas A. Rocheleau, and Donald J. Mer-lo are the inventors. Plaintiff Agrigenet-ics, Inc. is a Mycogen subsidiary. In a complaint filed in October 1996, Mycogen and Agrigenetics contend Monsanto Company, DeKalb Genetics Corporation, and Delta and Pine Land Company infringe the ’600 and ’862 patents, and that they are contributing to and inducing infringement of these patents. Defendants have answered denying the allegations and asserting affirmative defenses. Defendants also counterclaim for a declaratory judgment of non-infringement and invalidity of the ’600 and ’862 patents. On February 3, 1998, a jury returned a verdict finding that the defendants’ products do not literally infringe the contested claims of the ’600 or ’862 patents. The jury also found that the contested claims of the ’600 and ’862 patents are anticipated and therefore invalid because the subject matter was invented at Monsanto before the invention date of plaintiffs patents. The parties moved for judgment as a matter of law and have filed other post-trial motions. This is the court’s decision on all pending post-trial motions. I. FACTUAL AND PROCEDURAL BACKGROUND A. The Status of the Case The court draws the following facts from the evidence presented at trial. Plaintiff Mycogen Plant Science, Inc. is a Delaware corporation with its principal place of business in San Diego, California. Mycogen owns the ’600 patent and the ’862 patent, which are directed to a synthetic gene inserted into plants to make plants insect-resistant. Agrigenetics, Inc., a My-cogen subsidiary, is a Delaware corporation with its principal place of business in San Diego, California. In this opinion, the court refers to the plaintiffs collectively as “Mycogen.” Defendant Monsanto Company is a Delaware corporation with its principal place of business in St. Louis, Missouri. Defendant DeKalb Genetics Corporation is a Delaware corporation with its principal place of business in DeKalb, Illinois. Defendant Delta and Pine Land Company is a Delaware corporation with its principal place of business in Scott, Mississippi. In December 1998, Monsanto acquired De-Kalb which became a wholly-owned subsidiary of Monsanto. On October 22, 1996, Mycogen filed the complaint in this case contending defendants infringe and induce or contribute to infringement of Claims 1-24 of the ’600 patent and Claims 1-24 of the ’862 patent. Mycogen also alleged that defendants willfully infringe both patents. Defendants answered denying the allegations and asserting several affirmative defenses, including that Mycogen’s patents are unenforceable because Mycogen allegedly willfully misled the Patent and Trademark Office (“PTO”) by failing to disclose material information to the PTO, and that the ’600 and ’862 patents are invalid for failure to comply with 35 U.S.C. §§ 101, 102, 103 and 112. Aso, defendants counterclaimed that the ’600 and ’862 patents are invalid for failure to comply with 35 U.S.C. §§ 101, 102, 103 and 112, including for prior invention, lack of enablement, failure to disclose best mode, and indefiniteness. On September 30 and October 1, 1997, this court held the part of the trial necessary to construe disputed claim language of the ’600 and ’862 patents, in accordance with Markman v. Westview Instruments, Inc., 517 U.S. 370, 116 S.Ct. 1384, 134 L.Ed.2d 577 (1996). The court subsequently issued an opinion construing the patent claims. See Mycogen v. Monsanto, D. Del. C.A. No. 96-505-RRM, memo, opin., McKelvie, J. (December 29, 1997) (D.I.343). From January 20 to February 3, 1998, the court held a ten-day jury trial on the issues of infringement, willful infringement and invalidity. Before the close of evidence at trial, Mycogen withdrew its claims for willful infringement. On February 3, 1998, the jury returned its verdict. The jury found that defendants’ products do not literally infringe the asserted claims of the ’600 and ’862 patents. The jury also found the contested claims of the ’600 and ’862 patents are anticipated, and therefore, invalid because their subject matter was invented at Monsanto before the invention date of Mycogen’s patents. The jury did not enter a decision on whether Monsanto actively induced others to make, use, sell, or offer to sell infringing products, or whether Monsanto actively induced farmers to infringe by using infringing products. The jury did not reach a decision but noted “N/A” to the following questions: (1) whether any of the contested claims of the ’600 and ’862 patents are invalid because the specification of the patents would not have enabled a person of ordinary skill in the art as of September 9, 1988, to make use of the claimed invention without undue experimentation; (2) whether the ’600 and ’862 patents are invalid because the inventors failed to adequately disclose in the patent specification what they believed as of September 9, 1988, to be the best mode for practicing their invention; and (3) whether the ’600 and ’862 patents are invalid because they do not clearly and distinctly claim the subject matter of the invention. On February 5, 1998, the court entered judgment in favor of defendants. To better explain the court’s decision on the pending motions, the court first provides the reader with background on two scientific topics central to this case: (1) Bacillus thuringiensis, a naturally-occurring bacterium; and (2) genetic engineering. B. Background Information on Bacillus Thuringiensis The court draws the following facts from the court’s claim construction opinion and from the evidence presented at trial. Bacillus thuringiensis (“Bt ”) is a naturally-occurring bacterium found in soil. Bt possesses an unusual property; it produces a protein that kills certain crop-destroying insects. This protein is known as a “pestieidal protein toxin,” “pesticidal protein,” or “toxic crystal protein.” When eaten by certain insects, the protein dissolves the insects’ stomach linings, causing the insects to die. While the Bt protein is a natural pesticide, it is not harmful to humans, animals or beneficial insects like bees and ladybugs. The Bt protein is particularly deadly for insects like the European corn borer. This worm-like insect feeds on corn plants, eating its way into stalks and ears. The European corn borer can kill a plant outright or dramatically reduce the size and number of kernels that grow on an ear. This pest costs American farmers as much as an estimated $1 billion a year in lost crops. For years, farmers have been spraying their crops with pesticides like the Bt protein as well as other chemicals. Spraying, however, is not always effective because some insects, including the European corn borer, tunnel into plants soon after they hatch, or stay on the underside of leaves, where the spray does not reach them. In addition to being ineffective, spraying adds to farmers’ costs and the spraying of some pesticides raises environmental and health concerns. Scientists have long considered the idea of introducing genes from different organisms into crops and livestock. Developments in genetic engineering focused the scientific community’s attention on whether plants could somehow be genetically-modified to resist attack by insect pests. Advances in agricultural biotechnologies made it possible to create plants which produce Bt pesticidal proteins. Thus, these genetically-modified plants have their own built-in, or endogenous, protection from insects. Issues related to these biotechnological advances are at the heart of this case. Initially, scientists experimented with inserting into plant cells the native Bt gene that produces the Bt pesticidal protein. The native Bt gene refers to the naturally-occurring gene as found in the bacterium. While scientists succeeded in inserting native Bt genes into plant cells, they found that these new genetically-modified plants were not producing enough Bt pesticidal protein to kill insects. In scientific terms, the level of expression of the native Bt genes inserted into the plants was too low. To solve the problem of low Bt expression, scientists devised ways to increase the level of Bt expression in plants. They eventually succeeded by modifying the native Bt gene, as detailed below. Scientific success led to commercial success. The U.S. Environmental Protection Agency gave its first approval to a plant genetically-engineered to biologically control insects on May 5, 1995, when it approved a genetically-modified potato. By 1996, the EPA approved insect-resistant corn for commercial use. In 1996, U.S. farmers planted very few genetically-modified crops. By 1999, genetically-modified corn accounted for no less than one-fourth of the corn grown by U.S. farmers. See Carol Kaesuk Yoon, “Pollen From Genetically Altered Corn Threatens Monarch Butterfly, Study Finds,” New York Times, May 20, 1999 (estimating that in 1999, Bt corn to be cultivated on an estimated ten million to twenty million acres out of an eighty million acre corn crop nationwide); “Doubling of Land Area Growing Genetically Modified Crops,” Agenee France-Presse, February 26,1998, (estimating that in 1998, genetically-modified corn to be cultivated on eight million hectares [19.75 million acres], chiefly in the United States); see also “Food for Thought,” Economist, Jun. 19, 1999, (estimating that genetically-modified crops account for as much as 55% of U.S. soybean, 50% of U.S. cotton and 40% of U.S. corn production.). The patents-in-suit involve a method aimed at solving the problem of low Bt expression in genetically-modified plants. To help the reader understand this method and the issues underlying this case, the court provides the following background information on genetic engineering. C. Background Information on Genetic Engineering Organisms, like plants and animals, are made up of cells. Genes are units of DNA (deoxyribonucleic acid) which encode the necessary information for cells to reproduce and to produce specific proteins. Genes are comprised of DNA, an acronym for deoxyribonucleic acid. DNA consists of two long chains or strands that wrap around each other in a shape known as a double-stranded spiral helix. Visually, a molecule of DNA resembles a twisted ladder. The sides of the ladder are connected by rungs made up of pairs of molecules called nucleotides or bases. Four nucleotides, adenine (“A”), guanine (“G”), cytosine (“C”) and thymine (“T”), form the particular DNA make-up of genes. A particular DNA molecule can be graphically represented by listing the nucleotide sequences making up that DNA molecule. Because of the nucleotides’ chemical make-up, A will only pair with T, and C will only pair with G. This strict complementary pairing means that the order of the nucleotides on one side of a DNA rung determines the order on the other side of the rung. Therefore, each rung of the ladder is composed of one pair consisting of A and T, or C and G. Each rung is called a nucleotide pair, and the order in which these nucleotide pairs appear on the DNA ladder constitutes the genetic code for the cell. DNA directs cells to make proteins through a two-step process of transcription and translation. In the first step, transcription, information is transferred from DNA to an RNA, or ribonucleic acid, molecule. RNA that codes for a protein is called messenger RNA (“mRNA”). RNA is a long single strand of linked nucleotides similar to DNA, except RNA contains the nucleotide Uracil (“U”) in place of Thymine. In transcription, specific nucleotide sequences on the DNA determine where the RNA copy begins and ends. In the second step, translation, the nucleotide sequence of the mRNA is translated into the amino acid sequence of the corresponding protein. For this translation work, a complex structure known as a ribosome reads the mRNA nucleotide sequence and translates it into amino acids. These amino acids are then assembled into proteins. In this way, ribosomes carry out protein synthesis. Ribosomes read a nucleotide sequence in sets of three nucleotides, known as codons. Each codon directs the ribosome to select a certain amino acid. For example, GCT is a codon directing the ribosome to select the amino acid, alanine. Just as nucleotides are the basic units of DNA, amino acids are the basic units of proteins. A protein can contain few or many amino acids. For example, some Bt pesticidal proteins contain more than 600 amino acids. Thus, a given series of codons specifies a sequence of amino acids comprising a particular protein. While there are 61 possible codons, there are only 20 amino acids. Some amino acids can be specified by more than one codon. In other words, one codon can be substituted for another in the gene without changing the amino acid and resulting protein. For instance, the amino acid, alanine, is specified by four different codons: GCT, GCG, GCC and GCA. Two very different series of codons could produce the exact same series of amino acids. In fact, most amino acids are specified or coded by more than one codon. Scientists employ special tables known as codon usage tables to determine the frequency with which certain codons appear in plants and other organisms. For example, Table 1 of the ’600 and ’862 patents contains a listing of all 20 amino acids along with the various codons which specify these amino acids. Table 1 then compares the frequency with which the codon appears in three different organisms: dicot plants, the Bt gene and monocot plants. The terms, “dicot” and “monocot,” are used frequently in this opinion. These terms refer to two plant categories. A plant is classified as monocot or dicot depending on how many leaves it produces when it sprouts from the seed. If the plant has only one leaf when it first emerges from the soil, it is a monocot; if the plant has two leaves, it is a dicot. For example, tomato, tobacco and cotton are dicots; corn, barley, rice and wheat are monocots. Knowing that different codons can specify the same amino acid, scientists attempted to solve the problem of low Bt expression in plants by changing the codons in the native Bt gene, without changing the resulting amino acids. Scientists recognized that organisms prefer certain codons over others for specifying particular amino acids. For example, while the amino acid, alanine, is specified by four different co-dons, GCG, GCA, GCT and GCC, the co-dons appear disproportionately. To illustrate this point, GCA appears 50% of the time that alanine is specified in Bt genes, while GCG only appears 12% of the time that alanine is specified in Bt genes. . Scientists sought to create a Bt gene that would have a codon frequency more like plants, but produce high levels of pes-ticidal Bt protein. The following table illustrates how scientists approached their goal of making the Bt gene more plantlike. The table reports the frequency of codon usage for the amino acid, alanine, in dicot genes, Bt genes and monocot genes. The number represents the percent of the time a codon appears in a host when alanine is specified. As seen above, GCA appears 50% of the time in the Bt gene when alanine is specified. However, in a dicot plant gene, GCA only appears about 25% of the time. Two other alanine codons, GCC and. GCT, appear more frequently in dicot genes (27% and 42% respectively) than they do in Bt genes (6% and 32% respectively). Thus, by changing GCA codons in the Bt gene to either GCC or GCT, the new Bt gene becomes more plant-like because dicot plants prefer GCC or GCT over GCA. Modifications, such as these, result in higher expression of the pesticidal Bt protein in the plants containing this synthetic Bt gene, compared to those plants containing the native Bt gene. Scientists also discovered that the nucleotide sequence AT appears in Bt genes more frequently than it appears in plant genes. They thought that this factor, along with the existence of other identifiable sequences, might be the cause -of low Bt expression in plants. Who made this discovery, when it was made and how this discovery was used to design an insecticidal Bt gene are all key elements of this case. D. Mycogen’s Patents 1. General Background on the ’600 and ’862 Patents As explained at the outset, this case involves two Mycogen patents: the ’600 and the ’862 patents. The court offers brief background information on another Mycogen patent, U.S. Patent No. 5,380,831 (“the ’831 patent”), which is closely-related to the ’600 and ’862 patents. The ’831 patent is the predecessor patent to the ’600 and ’862 patents. All three patents are entitled “Synthetic Insecticidal Crystal Protein Gene.” The specifications for all three patents are almost identical and the three patents share many terms and phrases. The first page of the ’600 patent indicates it is a continuation-in-part of the ’831 patent, while the first page of the ’862 patent indicates it is a division of the ’831 patent. See Mycogen v. Monsanto, C.A. No. 96-505-RRM, memo, opin., McKelvie, J. (D.Del. December 29, 1997) (D.I.343) at 4-5. In broad terms, the ’831 patent claims a method of designing a synthetic Bt gene to make plants insect-resistant. Expanding on the ’831 patent, the ’600 patent claims a method of designing a synthetic Bt gene which includes the following four steps: (a) Analyzing the coding sequence of the Bt gene; (b) Modifying the Bt gene; (c) Inserting the synthetic Bt gene into a plant cell; and (d) Maintaining the plant cell under conditions suitable to allow replication. The ’862 patent claims the plant cell produced by the method disclosed in the ’600 patent. Thus, all three patents are based on the same concept of modifying Bt genes. The ’600 and ’862 patents are continuations-in-part of the ’831 patent, as represented in the chart below: The effective filing date for both the ’600 and ’862 patents is September 9, 1988, the filing date of U.S. Application No. 242,282. The inventions claimed in the ’600 and ’862 patents were constructively reduced to practice as of the filing date of this application. At that time, the inventions had not been actually reduced to practice. On October 22, 1996, the Patent and Trademark Office issued the ’600 and ’862 patents to Mycogen, as assignee. The abstract of both patents reads: Synthetic Bacillus thuringiensis toxin genes designed to be expressed in plants at a level higher than naturally-occurring Bt genes are provided. These genes utilize codons preferred to highly expressed monocot or dicot proteins. 2. The Specifications of the ’600 and ’862 Patents The patent specifications for the ’600 and ’862 patents discuss the use of preferred codons to make the synthetic Bt gene more plant-like. Table 1 of both patents is a codon usage table for dicot proteins, Bt proteins, the synthetic Btt gene and monocot proteins. (Btt refers to Bacillus thuringiensis var. tenebrionis, a strain of Bt bacterium from which the synthetic Bt gene was made.) At column 22, lines 19 to 44 of the ’600 patent, and at column 21, line 53 of the ’862 patent, the specifications give an example of using preferred codons to design a synthetic Btt gene. The specifications read, in relevant part, “[i]n designing a synthetic gene encoding the Btt crystal protein, individual amino acid codons found in the original Btt gene are altered to reflect the codons preferred by dicot genes for a particular amino acid.” The specifications also discuss removing codon sequences believed to inhibit Bt expression. For example, column 4, lines 17 to 23 of both patents state: [Consideration is given to the percentage G + C content of the degenerate third base (monocotyledons appear to favor G + C in this position, whereas dicotyledons do not). It is also recognized that the XCG nucleotide is the least preferred codon in dicots whereas the XTA codon is avoided in both monocots and dicots. At column 10, line 67 of both patents, the specifications further state that “[i]n dicots, XCG is always the least favored codon, while in monocots this is not the case. The doublet TA is also avoided in codon positions II and III in most euka-ryotes, and this is true of both monocots and dicots.” A eukaryote is an organism whose cells have a nucleus containing the genetic material, surrounded by cytoplasm, contained within a cell membrane. Examples include animals, plants, protozoa, and fungi. In eukaryotes, the DNA is packaged in chromosomes in the nucleus. Prokaryote refers to a single-celled organism with no nucleus, like bacteria. The DNA of proka-ryotes, usually a circular loop, is not separated into chromosomes. The specifications of both patents, at column 12, lines 9 to 12, state that “[i]n designing a synthetic gene for expression in plants, attempts are also made to eliminate sequences which interfere with the efficacy of gene expression,” such as the plant polyadenylation signal sequence AA-TAAA. The term “plant polyadenylation signal sequence,” or “polyA sequence,” refers to one way plants read certain nucleotide sequences to terminate mRNA synthesis. A plant cell naturally reads polyadenylation signal sequences as a termination signal while a bacterium, like Bt, does not. Thus, a plant cell might misread a polyade-nylation signal sequence in the Bt gene and terminate the synthesis of mRNA prematurely. In this case, an incomplete protein results. Beginning at column 23, line 58 of the ’600 patent and at column 23, line 18 of the ’862 patent, the specifications provide that “an elevated A+T content with the Btt coding region may be contributing to a low expression level in plants. Consequently, in designing a synthetic Btt gene, the A+T content is decreased to more closely approximate the A+T levels found in plant proteins.” Additionally, the specifications state that “the natural Btt gene is scanned for sequences that are potentially destabilizing to Btt RNA. These sequences, when identified in the original Btt gene, are eliminated through modification of nucleotide sequences.” The specifications identify “plant polyadenylation signals” including “AATAAA, AATGAA, AATAAT, AATATT, GATAAA, [and] AA-TAAG” as potentially destabilizing sequences. ATTTA is not identified as a plant polyadenylation signal on this list. 3. The Claims of the ’600 and ’862 Patents The claims of the ’600 patent are directed to methods of designing a synthetic Bt gene by modifying the coding sequence of a Bt gene causing it to be more highly expressed in plants; inserting this synthetic gene in a plant cell; and maintaining that cell. The claims of the ’862 patent are directed at the resulting plants, plant cells, and its progeny plants, cells and seeds. The ’600 patent consists of twenty-four claims. They may be organized into four sets of six claims each. The first set of claims consists of claims 1-6; the second set, 7-12; the third set, 13-18, and the fourth set, 19-24. (A table depicting highlights of the ’600 patent is provided below.) The first claim of each set, that is, Claims 1, 7, 13 and 19, discloses a method of designing a synthetic Bt gene. The claimed method involves four steps: (a) an “analyzing” step; (b) a “modifying” step; (c) an “inserting” step; and (d) a “maintaining” step. Claim 1 is representative of all four sets. It reads as follows: A method of designing a synthetic Bacillus thuringiensis gene to be more highly expressed in plants, comprising the steps of: (a) analyzing the coding sequence of a gene derived from a Bacillus thurin-giensis which encodes a pesticidal protein toxin; (b) modifying a portion of said coding sequence to yield a modified sequence which contains a greater number of co-dons preferred by the intended plant host than did said coding sequence prior to modification, said modification comprising reducing the number of codons having CG in codon positions II and III in a region between plant polyadenylation signals in said coding sequence; (c) inserting said modified sequence into the genome of a plant cell; and (d) maintaining said plant cell under conditions suitable to allow replication of said plant cell to produce additional plant cells having said modified sequence in the genome of said additional plant cells, wherein said synthetic Bacillus thuringiensis gene is expressed to produce a pesticidal protein toxin. Claims 7, 13, and 19 are identical to claim 1, except for step (b) which differs. How step (b) differs is explained below. The second claim of each set, Claims 2, 8, 14, and 20, claims the DNA coding sequence produced by the method disclosed in the first claim of the set. Claim 2 is representative of all four sets. It reads as follows: A DNA coding sequence produced by: (a) analyzing the coding sequence of a gene derived from a Bacillus thurin-giensis which encodes a pesticidal protein toxin; and (b) modifying a portion of said coding sequence to yield a modified sequence which contains a greater number of co-dons preferred by the intended plant host than did said coding sequence, said modification comprising reducing the number of codons having CG in codon positions II and III in a region between plant polyadenylation signals in said coding sequence. Again, Claims 8, 14 and 20 are identical to Claim 2, except for differences in step (b), described below. The third claim of each set, Claims 3, 9, 15, and 21, claim the method described in the first claim, limited by the requirement that “at least about 32% of the codons in the coding sequence of the native Bt gene have been modified.” The fourth claim of each set, Claims 4, 10, 16, and 22, claims the method described in the first claim, limited by the requirement that “about 11% of the nucleotides in the coding sequence of the native Bt gene have been changed.” The fifth and sixth claims in each set, Claims 5-6, 11-12, 17-18, and 23-24, claim the DNA sequence described in the second claim, limited by the same two requirements set out by the third and fourth claim of each set as explained above. Step (b) of Claims 1-2, 7-8, 13-14 and 19-20 contains two limitations which apply to all four sets of claims. Each claim contains either a “greater number” limitation (Claims 1-2, and 13-14) or a “frequency” limitation (Claims 7-8, and 19-20), and each claim contains an “XCG” limitation (Claims 1-2, and 7-8) or an “AATGAA” limitation (Claims 13-14, and 19-20). The “greater number” limitation is the phrase appearing in Claim 1. This refers to “a modified sequence which contains a greater number of codons preferred by the intended plant host.” The “XCG” limitation also appears in Claim 1. This refers to a modification comprising “reducing the number of codons having CG in codon positions II and III in a region between plant polyadenylation signals in said coding sequence.” In step (b) of Claim 19, the “frequency” and “AATGAA” limitations appear, instead of the “greater number” limitation and the “XCG” limitation. Claim 19(b) reads as follows: (b) modifying a portion of said coding sequence to yield a modified sequence which has a frequency of codon usage which more closely resembles the frequency of codon usage of the plant in which it is to be expressed than did said coding sequence prior to modification, and wherein said modification results in fewer occurrences of the sequence AAT-GAA in said modified sequence than in said coding sequence. As for the ’862 patent, Claims 1, 7, 13 and 19 claim the plant cells produced by the methods disclosed in the ’600 patent. Claims 2-5, 8-11, 14-17, and 20-23 are dependent claims. Claims 2-5 are representative of these dependent claims: Claim 2. Progeny cells of the cell of Claim 1. Claim 3. A plant comprising progeny cells according to Claim 2. Claim 4. A progeny plant of the plant of Claim 3. Claim 5. A seed of a plant of Claim 3 or Claim 4. E. Monsanto’s Patent At trial, Monsanto argued that Monsanto scientists David Fischhoff and Fred Perlak invented the invention before Michael Adang and Elizabeth Murray invented it. Accordingly, the court provides background on Fischhoff and Perlak’s work leading to their invention. On February 24, 1989, Monsanto filed a patent application, U.S. Patent Application Serial No. 315,355, with the PTO. This application eventually matured into the ’365 patent. Fischhoff and Perlak prepared four different draft applications on September 19, 1988, October 5, 1988, December 7, 1988 and February 7, 1989 before Monsanto filed the final application with the PTO. The December 7, 1988 draft application was the first to include a codon usage table. The ’365 patent is entitled “Synthetic Plant Genes.” According to the abstract, it discloses a “method for modifying structural gene sequences to enhance the expression of the protein product” and “novel structural genes which encode insecticidal [.Bt] proteins.” The method disclosed in the ’365 patent increases production of the Bt toxin by replacing Bt gene sequences believed to reduce Bt expression in plants with sequences believed to enhance Bt expression in plants. Thus, the ’365 patent involves the selective modification of Bt genes to make them compatible with plants, thereby resulting in insect-resistant plants. In a continuation application, dated April 26, 1995, Monsanto distinguished its invention from Mycogen’s ’831 patent by emphasizing that Monsanto’s invention focused on making changes in the 240 region of the Bt gene. Monsanto stated that its invention was “directed to the discovery that when one eliminates certain sequences and when one increases plant preferred codons, that some changes are more important than others and that certain locations in the Bt gene are more important to change to achieve Bt gene expression than other locations.” Monsanto compared this to the ’831 patent which “does not distinguish any region of the Bt gene from any other region of the Bt gene.” The PTO issued the ’365 patent on March 19,1996. In terms of commercial applications, Monsanto designs various insect-resistant gene products and cells based on the invention claimed in the ’365 patent. These Monsanto products, at issue in this case, include: NewLeaf® Potato, Cry3B2 corn, Cry2Bcorn, CrylA(c)/CrylF cotton, Stone-ville cotton, and IrmI corn gene products. Monsanto has licensed its YieldGard® Corn Products, also at issue in this case, to third parties, including Cargill Hybrid Seeds, DeKalb, Golden Harvest Seeds, Inc., Northrup King Co., and Pioneer Hi-Bred Int’l. F. Claim Construction The court has issued a memorandum opinion setting forth its construction of phrases in the claims of the ’600 patent and ’862 patent. Accordingly, it will only briefly summarize its decision here. See Mycogen v. Monsanto, C.A. No. 96-505-RRM, memo, opin., McKelvie, J. (D.Del. December 29, 1997) (D.I.343). With respect to the claims of the ’600 patent, the court found: 1. The phrase “ ‘more highly expressed,’ refers to the level of messenger RNA produced by the synthetic gene.” 2. The phrase “ ‘derived from a Bt,’ means taken, obtained, received, traced, replicated, or descended from Bt.” 3. The word “ ‘maintaining,’ means keeping the plant cell in tissue or as part of a plant, so long as conditions continue that allow the plant cell to divide and multiply.” 4. The phrase “ ‘greater number of codons preferred,’ is satisfied where the newly-created synthetic gene has a higher number of those codons whose frequency in the native Bt gene was lower than their frequency in the intended plant host, and where the synthetic gene has an overall distribution of codon usage that is closer to that of the intended plant host.” 5. The phrase “ ‘said modification comprising reducing the number [of XCG codons],’ means only that the overall modification must include a reduction in the number of XCG codons, not that each change of an XCG codon to a non-XCG codon must satisfy the ‘greater number’ or ‘frequency’ limitation.” The court also construed certain phrases and words in the claims of the ’862 patent. The court determined that the claim construction given for the ’600 patent applied to the same phrases and words used in the ’862 patent. Additionally, the court construed the phrase, “ ‘progeny cells,’ to refer to multiple generations of cells,” and the phrase “ ‘progeny plant’ to refer to plants that encode a pesticidal protein toxin.” G. Jury Trial From January 20 to February 3, 1998, the court held a ten-day jury trial on the issues of infringement and invalidity. The court summarizes the testimony and other evidence below. 1. Mycogen’s case-in-chief Among the issues Mycogen set out to prove at trial is that scientists at Agrigen-etics first conceived of a method to modify Bt genes so that these modified Bt genes could be put into plants to make them insect-resistant. Mycogen asserted that scientists at Agrigenetics conceived of the inventions claimed in the ’600 and ’862 patents in November 1985, earlier than Monsanto conceived of its inventions claimed in its ’365 patent. Similarly, Mycogen asserted that Agri-genetics was the first to file a patent application for this invention and that Agrigenetics exercised the legally-required diligence from the time of the invention’s conception to the filing of the patent application with the PTO. Myco-gen also asserted that while Monsanto got good results in its Bt gene modification experiments, Monsanto did not know the reason for these good results. In other words, Monsanto did not know the recipe for its invention. Mycogen asserted Monsanto derived the subject matter claimed in the ’600 and ’862 patents from Agrigenetics and that Monsanto placed a plant preferred codon table in its patent application in response to information Monsanto obtained improperly from the Agrigeneties’ patent application. Monsanto reviewed this application on November 1,1988 as part of Monsanto’s overall evaluation of Agrigenetics’ assets because Monsanto wanted to make an offer to purchase Agrigenetics. While Monsanto received Agrigenetics’ permission to review its patent application, Monsanto did so with the agreement that the application information would not be used to enhance Monsanto’s own efforts in developing a Bt gene. Monsanto completed its evaluation and made an offer which Agrigenetics refused. Mycogen asserted that Monsanto violated this agreement by using the confidential information in the patent application. Mycogen also asserted that prior to placing a plant preferred codon usage table in its patent application, Monsanto had abandoned the idea of modifying the Bt gene with plant preferred codons. As its first witness in its infringement case, Mycogen called Dr. Jerry Caulder, Mycogen’s first president and chief executive. Caulder testified about his role in developing Mycogen into a biotechnology company offering alternatives to the use of chemicals as a method of insect control in agricultural production. According to Caulder, Mycogen scientists explored the creation of insect-resistant genes as one such alternative. Caulder testified that one of the reasons Mycogen acquired Agri-genetics in 1992 was because Agrigenetics scientists had worked on inserting genes into plants and Mycogen needed to find a method for inserting genes into seed. On cross-examination, Caulder testified that while he did not know Mycogen’s “exact progress,” he was aware that Myco-gen was working in the area of corn transformation capability in 1994. According to Caulder, “corn transformation capability” means “the ability to transform corn” by, for example, inserting a Bt gene into corn seed. DeKalb’s counsel asked Caulder about an August 8, 1994 memorandum written by Leo Kim, Mycogen’s head of research, purporting to discuss things My-cogen wanted to accomplish, among them to “[ojbtain corn transformation capabilities by internal development, license or contract.” After reviewing the memorandum, Caulder testified that “we [Mycogen] were obviously working toward it [obtaining corn transformation capabilities by internal development, license or contract]. [I]n a very small company, we don’t care if we develop it internally, license it or contract, as long as we have the ability to do it.” Mycogen next called Dr. Joseph 0. Fal-kinham, III, a professor of microbiology and genetics at Virginia Polytechnic Institute. Falkinham first testified about genetics principles and methods for inserting Bt genes into plants. He testified about two methods of inserting Bt genes into plants: (1) microprojectile bombardment, which uses a device known as a gene gun, and (2) electroporation. According to Fal-kinham, a gene gun literally “shoots” Bt genes into cells. Electroporation involves adding an electric charge to a solution containing plant cells which renders them permeable to Bt genes. Falkinham testified about the ’600 and ’862 patents. According to Falkin-ham, these patents teach that the problem of low Bt expression “can be overcome by making the Bt genes use codons more like a plant.” Scientists can make a Bt gene sequence more plant-like by changing the codons without changing the amino acid in the protein. Falkinham testified that these two patents teach that “there are some codons that very rarely occur in plant genes.” He identified these as codons ending with C and G. Falkinham referred to these codons as “XCG,” where the variable X represents either A, T, G, or C. According to Falkin-ham, the ’600 and ’862 patents teach that gene codons can be made more plant-like by eliminating XCG sequences and polya-denylation sequences. Falkinham testified that XCG sequences should be eliminated because XCG codons rarely occur in plants. According to Falkinham, the patents teach that polyadenylation sequences, also known as polyA sequences, defined as “short sequences” consisting of “about six nucleotides,” should be eliminated because, while polyadenylation sequences are used to code for amino acids in bacteria like Bt, they cause premature termination of protein synthesis in plants. On cross-examination, Falkinham also testified that Claims 1 through 12 of both patents do not require removal of the polyadenylation sequence AATGAA. Falkinham testified that in his opinion, defendants’ commercial genes and gene products infringe the ’600 and ’862 patents. According to Falkinham, the process for designing Monsanto’s BollGard® cotton gene infringes claims of the ’600 patent. Specifically, the process infringes all the elements of Claim 2 of the ’600 patent because Monsanto undertook a “back translation process” which satisfies Claim 2’s analyzing and modifying steps. A “back translation process” involves deriving all possible DNA sequences based on the known amino acid sequence for a protein. Falkinham testified that the BollGard® cotton gene sequence contains: (1) a greater number of codons preferred by the intended plant host as required by Claim 2; and (2) a reduced number of XCGs. According to Falkinham, about 32% of the codons in the BollGard® cotton gene have been changed in a manner that infringes Claims 5, 11, 17 and 23 of the ’600 patent. At least 11% of the nucleotides in the BollGard® cotton gene have been changed in a manner that infringes Claims 6, 12, 18 and 24 of the ’600 patent. Falkinham testified that the BollGard® cotton gene has an AATGAA sequence removed, which infringes Claims 14 and 20 of the ’600 patent. He also testified that the BollGard® cotton gene has a frequency of codon usage more closely resembling a plant which infringes Claim 8 and 20 of the ’600 patent. In sum, Falkinham testified that the Boll-Gard® cotton products, include the Boll-Gard® cotton gene and cells, infringe Claims 2, 5, 6, 8, 12, 14, 17, 18, 20, 23 and 24 of the ’600 patent. According to Falkinham, the BollGard® cotton gene and gene products infringe Claims 1, 2, 3, 4, 5, 7, 8, 9,10,11,13 and 14 of the ’862 patent. According to Falkinham, Monsanto’s YieldGard® corn gene, NewLeaf® potato gene, Northrup King Bt 11 event gene, Stoneville cotton gene and Monsanto’s and . Delta’s gene products all infringe claims of the ’600 and ’862 patents. Specifically, the NewLeaf® potato gene and potato products infringe Claims 2, 5, 6, 8, 11 and 12 of the ’600 patent and Claims 1, 2, 3, 4, 5, 7, 8, 9, 10 and 11 of the ’862 patent. The Northrup King Bt 11 event gene and plants infringe Claims 2, 5, 6, 14, 17, 18, 8, 11, 12, 20, and 23 of the ’600 patent and Claims 1-5, 7-11, 13-17 and 19-23 of the ’862 patent. The Stoneville cotton gene and plants infringe Claims 2, 5, 6, 8, 11 and 12 of the ’600 patent and Claims 1-5 and 7-11, 13-17 and 19-23 of the ’862 patent. According to Falkinham, DeKalb’s Bt gene and gene products, (DEKALBt™ Corn Product) including seeds, infringe Claims 2, 5, 6, 8, 11 and 12 of the ’600 patent and Claims 1-5, 7-11 of the ’862' patent. Falkinham testified that the defendants’ noncommercial gene and gene products infringe claims of the ’600 and ’862 patents. Specifically, Monsanto’s noncommercial CrylA(c) and CrylF products and genes infringe Claims 1-24 of the ’600 patent and Claims 1-3, 6, 7-9, 12,13-15,18,19-21 and 24 of the ’862 patent. Monsanto’s noncommercial IRM1 products and genes infringe Claims 1-12 of the ’600 patent and Claims 1-3, 6, 7-9 and 12 of the ’862 patent. Falkinham testified that Monsanto’s noncommercial Cry2B products and genes infringe Claims 2, 5, 8, 11, 12, 14, 17, 18, 20, 23 and 24 of the' ’600 patent and Claims 1-5, 7-11, 13-17, 19-23 of the ’862 patent. Monsanto’s noncommercial P2A and P2B products and genes infringe claims of the ’600 patent and claims of the ’862 patent. Monsanto’s noncommercial 3B2 corn products and genes infringe claims of the ’600 patent and claims of the ’862 patent. Mycogen called Dr. Elizabeth Murray to testify. By way of background, Agrigenet-ics researched the possibility of increasing insect resistance in plants by creating a synthetic Bt gene during the mid- to late-1980’s. Two Agrigenetics scientists, Murray and Dr. Michael J. Adang, Murray’s supervisor, primarily carried out this research. They are co-inventors of the ’600 and ’862 patents. Adang, Murray and other Agrigenetics scientists working on Bt expression levels referred to their discoveries and documented their research in their laboratory notebooks and in various publications. Murray testified that she started working at Agrigenetics in October 1985, shortly after completing her Ph.D. dissertation at the University of Kansas. By this time, Agrigenetics had succeeded in putting native Bt genes into plants. However, the plants’ Bt gene expression was low. In November 1985, Murray and Adang discussed experiments she wanted to conduct for the purpose of identifying the reason for this low Bt gene expression. Murray told Adang she believed “the coding sequence itself of the Bt gene was the problem” and that they “would have to go through and modify the coding sequence of the Bt gene in order to improve its expression.” She and Adang decided to focus on modifying a specific region of the gene by changing the ratio of AT and GC without changing the resulting amino acid. At trial, Mycogen introduced into evidence a one paragraph abstract with an accompanying Agrigenetics “Manuscript and Abstract Review Form” to demonstrate that on November 8, 1985, Adang, Murray and other Agrigenetics scientists wrote an abstract for presentation at an April 1986 symposium at the University of California at Los Angeles. This abstract, entitled “Novel Applications of a Bacillus thuringiensis Crystal Protein for Insect Control,” reads in relevant part: A continuing challenge in controlling pest insects is the development of plants resistant or tolerant to insect attack. One approach to accomplishing this objective is to express proteins that are deleterious to insects in plants. Insect pathogens such as Bacillus thuringien-sis provide a source for these toxin genes.... We have observed significant levels of truncated B. thuringiensis peptides synthesized in callus and immature shoot tissue. Work is in progress to further evaluate the expression of this gene in tobacco and other plants. Murray testified that she had a “recipe” for modifying the Bt gene in 1985. According to Murray: [The] recipe was to analyze the sequence of the gene, to modify it to reflect the usage of the codons of a plant gene and to balance the ratios of occurrence of GC and AT, those two pairs. It was also to increase the expression of the RNA. And we included the idea that it had to express RNA as well as the two genes on either side of it, and we had the conception we should remove polyadeny-lation signals that were used in plants and, as part of that, we felt that we should include avoiding the codons that plants avoided using. Murray testified that the specific codons that “plants avoided using” referred to XCGs and CGs in general. She testified that she knew plants avoided using these codons based on her reading of an article published in FEBS Letters in March 1988 titled “Are Plant Genes Different?” by Grantley W. Lycett, et al. Murray cited the Lycett article on page 123 of her Ph.D. dissertation, “Molecular Biology of the Ri-cin [a castor bean protein] Multigene Family.” She successfully defended her dissertation in September 1985, just before starting at Agrigenetics. Murray testified that she believed she relied on a codon usage table published in the Lycett article for information she needed to modify the Bt gene. On cross-examination, Murray testified that from 1985 into 1987, she and Adang also tried to make the native Bt gene work in plants; Adang wanted to make “incremental improvements” to show that it worked. She testified that while she had the idea in 1985 to create a synthetic Bt gene by removing certain sequences of the gene to make it more plant-like, she did not write down, document or implement this idea until the summer of 1987. At that time, she began to create the codon usage table that became part of the ’600 and ’862 patents. On August 27, 1987, Murray made the first notations in her laboratory notebook about altering the coding sequence of the Bt gene. Murray wrote the “general idea is we should change the coding sequence of the Bt gene to make it look more like a plant gene.” On this same date, she also wrote in her laboratory notebook that “I learned how to use the computer to do an analysis of the codon usage.” According to Murray, she spent two days making the codon usage table that eventually appeared in the Mycogen patents. Murray testified that nothing in her laboratory notebook suggests she was working on codon usage tables from August 27, 1987 until January 19, 1988. On January 19, 1988, Murray first wrote about designing a synthetic gene in her laboratory notebook, noting “[w]e also discussed rebuilding the gene.” On cross-examination, Murray testified that at the time the Agrigenetics patent application was filed, she believed that the ATTTA sequence could contribute to RNA instability in the Bt gene. She testified that this finding had already been reported in the scientific literature. She testified that she “thought that [ATTTA] was one of the reasons the AT-richness of the genes might be unstable.” She testified that when she read the literature she was excited because someone else was “confirming [her] idea and showing that AT-richness RNA is very unstable.” DeKalb’s counsel asked Murray about a two-page Agrigenetics memorandum, dated February 29, 1988, from Les Hoffman to John Ingle. In this memorandum, Hoffman, an Agrigenetics scientist, wrote that he planned to “test the functionality of suspected AT-rich motifs in the Bt gene,” and that Murray favored the approach he proposed. Hoffman specifically identified the ATTTA sequence as a possible cause of mRNA instability, and referred to ATT-TA as a “ ‘sudden death’ sequence.” Hoffman also noted that: By identifying sequences which, when replaced, allow us to stabilize Bt RNA, we may be able to significantly increase Bt expression levels in plant cells without a complete gene reconstruction. This approach will require cooperation and a willingness to drop other avenues of research in the Bt area should “death sequence” elimination appear to be effective. On cross-examination, Murray testified that she had seen this memo in 1988 and that Hoffman, with whom she worked, referred to ATTTA as “the sudden death sequence.” According to Murray, she did not consider elimination of ATTTA to be the best mode of carrying out her invention in 1988 “[b]ecause if you modify a plant gene for codon usage, you have a [ tendency] to change those sequences anyway.” She testified that she “felt the broadest claim of the patent would be to overall change the AT richness of the gene, by changing the codon usage and ... it [ATTTA] was included within the original conception of the idea that ... these sequences would be changed.” On cross-examination, Murray testified that at a March 3, 1988 meeting held to discuss Bt, Agrigenetics scientists “designed the specific pieces” to create the synthetic gene using selected sequences and wrote out “the sequence” and “base pair changes that would go forward.” Murray wrote in her notebook that they “decided to push ahead with rebuilding [the] Btt gene based on codon usage tables” she had prepared. 2. Monsanto’s case-in-chief At trial, Monsanto asserted that Myco-gen’s patents are invalid due to prior invention under 35 U.S.C. § 102(g). According to Monsanto, the evidence shows that Fischhoff and Perlak invented its invention first, using a codon usage table prepared internally by Monsanto scientists. By October 30, 1986, Monsanto scientists had their blueprint to synthesize the Bt gene. By August 1988, they had their first successfully modified plant. To reinforce its invalidity due to prior invention argument, Monsanto asserted that Mycogen originally named four inventors for the patents at issue. In 1998, however, Mycogen dropped two of these inventors from the patents. According to Monsanto, Mycogen dropped these two inventors because the work they did on the Mycogen invention occurred in 1988, some three years after Mycogeris alleged 1985 date of conception. Monsanto also asserted that Mycogen’s patents are invalid due to lack of enablement. See 35 U.S.C. § 112 (requiring an inventor to disclose the method of making a claimed invention “in such full, clear, concise, and exact terms as to enable any person skilled in the art to which it pertains ... to make and use the same.”). According to Monsanto, the specifications of the patents would not enable a person of ordinary skill in the art as of September 9, 1988, to make use of the claimed inventions without undue experimentation. Monsanto denied Mycogen’s assertions that Monsanto derived the subject matter claimed in the Mycogen patents from My-cogen and that Monsanto placed a plant preferred codon table in its patent application in response to Monsanto’s review of the Agrigenetics patent application on November 1,1988. Just as Mycogen scientists experimented with ways to increase Bt expression levels in plants, Monsanto scientists conducted similar experiments. Two Monsanto scientists, Dr. David Fischhoff and Dr. Fred Perlak, headed this research effort. Just as Mycogen scientists documented their research in them laboratory notebooks and publications, so too did Monsanto scientists. Several witnesses referred to laboratory notebooks and publications to support their testimony. Monsanto called Perlak to testify. Per-lak began his testimony by discussing his work with Bt genes during the 1980’s. Perlak joined Monsanto in 1981. In that same year, Dr. Helen Whiteley, a researcher at the University of Washington in Seattle, made a major scientific breakthrough by isolating a piece of DNA and successfully moving it from Bt to E. coli, a strain of bacterium. Perlak testified that he met Fischhoff when both were working at Monsanto in 1988. Perlak’s role focused “on the Bt genes themselves” while Fischhoff focused on the “plant work.” Perlak testified that he and fellow Monsanto scientists conducted several experiments from 1984 through the early part of 1986 to attempt to get the native Bt gene to express in tobacco plants. These experiments failed; as Perlak testified, “we had come up against a very tough gene to express.” Similarly, experiments conducted with a truncated Bt gene were unsuccessful. As he testified, “we were still very disappointed in the overall levels of gene expression.” Perlak testified about a memorandum prepared by Fischhoff on October 30, 1986 and pasted into Fischhoff s laboratory notebook. According to Perlak, this memorandum represents a summary of the different ideas he and Fischhoff had for solving the problem of low Bt expression in plants. Perlak testified that the memorandum identifies “AT-rich regions” in the Bt gene sequence as destabilizing regions and that it specifically refers to the sequence ATTTA. Perlak testified that the memorandum defines “polyadenylation signal sequences as the consensus sequence AATAA,” and “variance[s]” of this sequence. Perlak testified that the definition of polyadenylation signal sequences for plants means “six nucleotides” containing “at least five A or T residues.” According to Perlak, “if one out of the five [in a sequence] is AG or AC, it still fits into the definition of a potential plant polyadenylation signal sequence.” Perlak testified that his definition of polya-denylation sequences encompasses the AATGAA sequence. Perlak testified that this memorandum lists two approaches to solving the problem of getting increased Bt expression in plants. One approach involves identifying and modifying the most AT-rich regions of the gene sequence because these regions cause instability in plant cells. The second approach involves looking at the entire gene sequence and creating a synthetic gene. As the memorandum explained, “[e]xtension of this strategy to total synthesis of Btk toxin gene, a predetermined sequence in base composition is also possible.” (Btk refers to a strain of bacterium known as Bacillus thuringiensis var. kurs-taki) Perlak testified that following the posting of this document to Fischhoff s laboratory notebook, he and Fischhoff began working on these two approaches for increasing Bt expression. According to Per-lak, he used a Monsanto-produced codon usage table, dated February 15, 1984, to make changes either to a portion of a gene sequence, or to an entire gene sequence. Perlak testified that the codon usage table on which he relied “was within Monsanto, published as an internal document, put together by a number of researchers, led [b]y Steve Rogers.” He testified that this codon usage table was “indispensable” for his work on the synthetic gene. Perlak testified that this table’s abstract identified certain codons, like CGX, XCG and XTA, as codons seldom found in plants. According to Perlak, this information guided him “away from using XCG, XTA, CGX [co-dons] and guide[d][him] toward plant preferred codons.” Perlak testified that he and Fischhoff worked on designing genes through “probably the end of August 1987.” Referring to his laboratory notebook, Perlak identified a September 8, 1987 summary statement describing a synthetic Bt gene they had designed. This statement noted the problem was “poor expression of Btk toxic gene plants ... [rjegions of AT-rich induced instability, ... [o]verall, AT too rich. Little used codons by plants found in the gene ... Solution is clear. Order a new gene synthesized to use plant preferred codons.” Perlak testified that he had “absolutely no doubt” that this solution entailed his using Monsanto’s codon usage table, dated February 16, 1984, to design the gene. According to Perlak, he made over 350 changes from the native Bt gene in his redesign effort. Perlak testified that by December 29, 1987, he had completed design of the coding region for a Bt toxin; which he described as the “genetic material that encodes the protein that kills insects.” According to Perlak, it “just need[ed] to be put in a vector that could transport this into a plant cell.” Vectors are DNA molecules used to carry or shuttle the gene into the plant. See, e.g., Ajinomoto Co. Inc. v. Archer-Daniels-Midland Co., 1996 WL 621837, *6 (D.Del. Oct.21, 1996). Perlak testified that Monsanto contracted with outside researchers in the United Kingdom to assemble the synthetic genes in three pieces following Perlak’s design. As the outside researchers assembled the pieces, they were shipped back to Perlak’s St. Louis laboratory where he put the three pieces together. Perlak testified that by May 9, 1988, Monsanto had designed three genes, known as the 5370, 5357 (also known as 5377), and 5383 genes. According to Per-lak, the design for the 5377 gene began in October 1986, when they “made the gene on paper.” According to Perlak, three Monsanto employees, Nancy Mathis, Gene Layton and Toni Armstrong, handled the responsibility of actually getting the synthetic genes into plants. Perlak testified that they succeeded in growing transgenic plants which were ready to be tested for increased Bt expression in early August 1988. Perlak recalled that around August 12, 1988, Dr. Roy Fuchs, the analyst responsible for this testing, told him: “Congratulations. You’ve done it. We now have plants that can express Bt at very high levels.” Perlak testified that the analyses showed the 5377 and 5383 genes were expressing Bt protein in plants. According to Perlak, the 5377 gene forms the basis of Monsanto’s current YieldGard® product and the 5383 gene forms part of the current BollGard® product. Perlak testified that the successful test results were obtained in advance of the filing date of the Mycogen patent applications on September 9, 1988. He also testified that he did not rely on any Myco-gen information for his work on the ’365 patent. On cross-examination, Perlak testified that he had no recollection of producing any draft applications of the ’365 patent prior to August 1988. When asked why he did not include a codon usage table in the ’365 patent application until December 1988, Perlak responded “[tjhere was no need” to put the codon usage table in the application because “[i]t was an inherent part of our invention. [There] was never any intent not to include it w