Full opinion text
OPINION FARNAN, Chief Judge. TABLE OF CONTENTS I. INTRODUCTION.541 A. Description of Parties.•.542 B. Jurisdiction .542 II. SCIENTIFIC BACKGROUND.542 A. Basic Concepts Relating to Gene Regulation .542 1. DNA, RNA, Transcription and Translation.543 2. Differences Between Prokaryotes and Eukaryotes.544 3. Antisense.544 B. Antisense Experimentation in Dr. Inoyue’s Lab.544 C. Dr. Izant and Dr. Weintraub’s Work in Antisense Technology.546 D. The Antisense Work of Other Scientists. 546 E. The Enzo Patent Prosecution. 547 1. Patent Applications.547 2. Prosecution History.547 3. Dr. Inouye’s Actions During Prosecution.547 F. The Calgene Patent Prosecution .548 G. Prior Litigation Between Enzo and Calgene.548 II. INFRINGEMENT.549 A. Establishing an Infringement Claim.549 B. The’931 Patent.550 1. Claim interpretation.550 a. Claim 1 of the ’931 Patent .550 b. Claim 3 of the ’931 Patent .553 c. Claim 5 of the ’931 Patent .553 d. Claim 7 of the’931 Patent .554 e. Claim 34 of the ’931 Patent .554 f. Claim 66 of the ’931 Patent .554 g. Claim 73 of the ’931 Patent .554 h. Claim 74 of the ’931 Patent .555 2. Literal Infringement of Enzo ’931 Patent.555 a. Claim 1 of the ’931 Patent .555 b. Claim 3 of the ’931 Patent .557 c. Claim 5 of the ’931 Patent .557 d. Claim 7 of the ’931 Patent .558 e. Claim 34 of the’931 Patent .559 f. Claim 66 of the ’931 Patent .559 g. Claim 73 of the ’931 Patent .559 h. Claim 74 of the ’931 Patent .559 3. Doctrine of Equivalents Infringement.559 C. The T49 Patent.560 1. Claim Interpretation.560 a. Claim 1 of the ’149 Patent .560 b. Claim 31 of the’149 Patent .561 c. Claim 61 of the ’149 Patent .561 d. Claim 93 of the ’149 Patent .562 e. Claim 125 of the ’149 Patent .562 f. Claim 159 of the T49 Patent .562 2. Literal Infringement of the T49 Patent.562 a. Claim 1 of the’149 Patent .562 b. Claim 31 of the’149 Patent .563 c. Claim 61 of the ’149 Patent .564 d. Claim 93 of the’149 Patent .564 e. Claim 125 of the ’149 Patent . 565 f. Claim 159 of the ’149 Patent .565 3. Infringement of the ’149 Patent under Doctrine of Equivalents.565 D. Conclusion .565 IV. INVALIDITY OF ENZO PATENTS .565 A.Enablement under 35 U.S.C. § 112.566 1. Arguments of the Parties.566 2. Establishing an Enablement Claim.566 3. Enablement of ’931 and T49 Patents .567 a. Level of Ordinarg Skill in the Art.567 b. Undue Experimentation.567 V. INVALIDITY OF CALGENE’S ’065 PATENT.569 A. Arguments of the Parties.569 B. Legal Standard.570 C. Discussion ..-.570 VI. ENZO’S MALICIOUS PROSECUTION CLAIM.570 A. Arguments of the Parties.570 B. Legal Standard.571 C. Discussion .571 VII. ATTORNEY’S FEES.'..571 VIII. CONCLUSION.571 I. INTRODUCTION This is a patent case involving genetic antisense technology. Plaintiff Enzo Bio-chem, Inc. (“Enzo”) brought this action against Defendant Calgene, Inc. (“Calgene”) for infringement of two patents for which it is the exclusive licensee (D.I.363). Enzo claims that Calgene infringes United States Patent Number 5,190,931 (the “ ’931 Patent”) and United States Patent Number 5,208,149 (the “ ’149 Patent”) by its production of the FLAVR SAVR® brand tomato. Enzo also seeks a declaratory judgment finding Cal-gene’s patent, United States Patent Number 5,107,065 (the “Calgene ’065 Patent”) invalid and unenforceable on the grounds of misuse, anticipation and obviousness. Finally, Enzo alleges malicious prosecution by Calgene as a result of Calgene’s litigation against Enzo in California. (D.I. 1 at 2, 44-46). Defendant Calgene has counterclaimed, seeking a declaratory judgment that the ’931 Patent, the ’149 Patent and a third Enzo patent, United States Patent Number 5,272,-065 (the “Enzo ’065 Patent”) are invalid, unenforceable and not infringed. (D.I. 54 at 367). Calgene contends that Enzo’s patents are invalid on the grounds of non-enablement, anticipation, obviousness and inequitable conduct before the United States Patent and Trademark Office (“PTO”). Additionally, Calgene defends the validity of the Cal-gene ’065 Patent, although it alleges that the Court has no jurisdiction to decide the issue. (D.I.367). Both parties seek an award of a attorney’s fees, claiming that the case is exceptional. (D.I. 363; D.I. 369). In the first patent infringement action filed by Enzo against Calgene, Enzo alleged infringement of its ’931 Patent only. (D.Del. C.A. 93-110-JJF). In the second infringement action Enzo filed against Calgene, it alleged infringement of its ’149 Patent. (D.Del.C.A.94-57-JJF). Because both actions involved similar factual and legal issues, the Court ordered the actions to be consolidated on October 7,1994. (D.I.322). The Court bifurcated the liability and damages issues for purposes of trial and conducted a bench trial on the issues of infringement, willful infringement, validity, enforceability, and attorney’s fees in April, 1995. (D.I.464). Pursuant to Federal Rule of Civil Procedure 52, the Court issued an Opinion setting forth its findings of fact and conclusions of law. Shortly thereafter, the parties informed the Court of an inconsistency in its Opinion. In order to prevent confusion on appeal, the Court withdrew its Opinion. Since withdrawing its Opinion, the Court has conducted a full review of the record and re-read the briefs submitted. As a result of this review, the Court has determined that its claim interpretation analysis omitted a discussion of the meaning of the disputed term “complementary” in Claim 1 and Claim 34 of the ’931 Patent. In the instant Opinion, the Court will include a discussion of this issue in its claim interpretation analysis. This Opinion shall constitute the Court’s findings of fact and conclusions of law in this case, superseding any previous findings and conclusions. A. Description of Parties Enzo is a company which seeks to find and create new technologies for development into products with biomedical and other scientific applications. (Engelhardt Tr. at 680). Enzo is comprised of three wholly owned subsidiary companies, including: Enzo Labs, a full service clinical reference laboratory; Enzo Diagnostics, a company involved in developing technology to identify pathogens by genetic analysis; and Enzo Therapeutics, a development company. (Engelhardt Tr. at 679). Enzo is the exclusive licensee of the ’931 Patent, the ’149 Patent and the Enzo ’065 Patent. The ’931 Patent issued to Dr. Ma-sayori Inouye on March 2, 1993 and claims a method of controlling the function of any gene in any cell through genetic antisense. (PX 730). The T49 Patent issued to Dr. Inouye on May 4, 1993, and is an improvement patent claiming a method of genetic antisense in stable stem and loop structures. Dr. Inouye is also the inventor on the Enzo ’065 Patent, issued on December 21, 1993, which also claims a method of regulating genes through genetic “antisense” technology. Enzo licensed these three patents from the Research Foundation of the State of New York and paid approximately three-quarters of a million dollars for them. (En-gelhardt Tr. at 681). Calgene is an agricultural biotechnology company with offices and facilities in California, Illinois, Mississippi and Florida. (Knauf Tr. at 1849). Calgene was founded in 1980, and since that time has focused its business strategy on the use of transgenic plant technology in agricultural applications. (Knauf Tr. at 1852-53). Calgene’s genetically engineered products include vegetable oils, cottonseed and the FLAVR SAVR tomato. Calgene is the assignee of United States Patent Number 5,107,065, issued to Christine Shewmaker, et al., on April 21, 1992. The Calgene ’065 Patent claims antisense regulation of gene expression in plants. The technology of the Calgene ’065 Patent was critical in the development of Calgene’s FLAVR SAVR tomato, a product which boasts a delayed ripening process. (Knauf Tr. at 1858-61). B. Jurisdiction The Court has jurisdiction over the parties and the subject matter of this patent dispute pursuant to 28 U.S.C. § 1338(a) (1995). The Court has jurisdiction over the asserted counterclaims pursuant to 28 U.S.C. §§ 1338(a) and 2201(a) (1995). Additionally, jurisdiction is proper under 28 U.S.C. §§ 1331 and 1332 (1995). II. SCIENTIFIC BACKGROUND A. Basic Concepts Relating to Gene Regulation The patents involved in this litigation concern “gene regulation,” in which the function or “expression” of a gene is manipulated. Both parties presented expert testimony on the basic concepts and principles of gene regulation. The Court has based its findings of fact with respect to the underlying science on the testimony of the experts the parties presented at trial. Regardless of what knowledgeable scientists in the field might believe is the relevant science, the function of the Court is to make findings of fact and draw conclusions of law based only on the evidence presented at trial. Accordingly, from the record evidence, the Court understands the underlying science relevant to the instant patents as follows. 1. DNA, RNA, Transcription and Translation A “gene” is a “nucleotide sequence,” such as deoxyribonucleic acid (“DNA”), which provides a code for a certain characteristic of an organism. (Green Tr. at 92; Falkinham Tr. at 1426). DNA makes up the genes of virtually every organism, and the genes determine the characteristics of the organism. (Green Tr. at 92). A single strand of DNA is made up of subunits, termed “nucleic acids” or “bases”, which link together to form a long chain. (Falkinham Tr. at 1408-09). These subunits are Adenine, Thymine, Guanine and Cytosine. Depending on the sequence in which they occur, they define every protein in an organism. (Falkinham Tr. at 1410). Two single strands of DNA are complementary, and can link up according to “base pairing rules,” where their bases pair together to form a double helix. (Green Tr. at 94). The bases can only link together in a certain way. For example, Adenine can link only with Thymine, and Guanine can link only with Cytosine. (Green Tr. at 94; Falkinham Tr. at 1410, 1411-12). Thus, the sequence in which the bases occur on one strand of DNA will dictate the required sequence of the second strand if they .are to form a double helix. (Green Tr. at 94). Two strands linked together in this fashion are said to be “complementary” to one another. (Green Tr. at 94). DNA tells the cells what proteins to make through a two-step process of “transcription” and “translation.” (Green Tr. at 92, 95; Fal-kinham Tr. at 1411). In the first step, transcription, the DNA transfers information to an RNA polymerase molecule, which makes a “messenger RNA” (“mRNA”) from the DNA, which in turn shuttles that information out into the cell. The DNA double helix opens up to permit a single strand of RNA polymerase to attach to one of the DNA strands. (Falkinham Tr. at 1414-15). Like DNA, RNA is a long chain of linking subunits, except that RNA contains the subunit Uracil instead of Thymine. When the RNA polymerase links with the single strand of DNA according to base pairing rules, the RNA’s Uracil pairs with Adenine instead of the DNA’s Thymine. (Green Tr. at 95). The RNA does not arbitrarily attach to the DNA, however, but begins reading at a “promoter sequence” and stops at a “terminator sequence,” both specified by the nucleic acid. (Green Tr. at 99; Falkinham Tr. at 1413). The promoter is the portion of the DNA construct which facilitates the start of the transcription of the RNA. (Green Tr. at 114.; Falkinham Tr. at 1413). The transcription termination segment is a configuration of bases on the fragment of the DNA construct which signals the end point of the RNA molecule. (Green Tr. at 114; Falkinham Tr. at 1413). The genetic message “stops” at the terminator sequence or segment. (Falkin-ham Tr. at 1414). In the second step, translation, a ribosome attaches to the released mRNA to construct a protein from the information in the mRNA. (Green Tr. at 96-97). A protein is comprised of a series of amino acids, which are themselves comprised of a configurations of bases, similar to those found in DNA. (Green Tr. at 97). The ribosome reads the information in the mRNA to determine which amino acids, and ultimately which protein, it is to create. (Green Tr. at 97). During translation, as the mRNA transfers its information about the amino acids into the ribosome, another molecule, the transfer RNA (“tRNA”), brings one of these amino acids that the mRNA has called for into the ribosome. (Green Tr. at 98). A second tRNA will bring the next amino acid, which links to the first, and a third tRNA will bring the third, which links to the second, and so forth until a complete chain forming the protein identified by the information in the mRNA is created. (Green Tr. at 98). DNA and RNA may also form a “stem and loop” structure. A stem and loop structure is a single strand of nucleic acid that folds back onto itself, creating a double-stranded loop according to base pairing rules. (Engel-hardt Tr. at 811; Green Tr. at 96). The stem and loop structure is not permanent, but instead undulates by repeatedly forming and collapsing. (Engelhardt Tr. at 811). A AG measurement measures the stability of the stem and loop: the higher the negative ‘G, the more stable the stem and loop. (En-gelhardt Tr. 811). 2. Differences Between Prokaryotes and Eukaryotes The primary difference between proka-ryotic cells and eukaryotic cells is that a prokaryotic cell does not have a nucleus or nuclear membrane, while a eukaryotic cell does. (Falkinham Tr. at 1419). One result of this difference is that a prokaryotic cell can commence translation of an mRNA even before the transcription process has ended. (Falkinham Tr. at 1415). In other words, while the RNA polyermase is creating the mRNA at one end, the ribosome is reading the information in the mRNA on the other. (Falkinham Tr. at 1415). Unlike prokaryotic cells, however, the mRNA in eukaryotic cells cannot undergo transcription and translation at the same time. Transcription in eukaryotic cells occurs in the nucleus of the cell, but translation occurs in the cytoplasm of the cell, so that the mRNA must pass through the nuclear membrane between the two steps. (Falkin-ham Tr. at 1423-25). Another distinction between prokaryotes and eukaryotes is that eukaryotic RNA has “introns”. (Knauf Tr. at 1886). Introns are intervening sequences that appear in the middle of a gene, and are similar to “a sequence of nonsensical letters or words which disrupted the normal flow of a sentence”. (Falkinham Tr. 1423). Eukaryotes can “clip-out” these sequences and splice the ends of messages back together again. (Falkinham Tr. at 1423). 3. Antisense Antisense technology regulates the expression of a gene by inhibiting either the transcription or translation of the coding. (Falkinham Tr. at 1427). For example, in naturally occurring antisense, the “sense” element is the single strand of DNA which contains the code that is transcribed into the mRNA, and that DNA strand makes sense in terms of what the message has to contain. (Green Tr. at 102). The code of the complementary strand of DNA would not make sense in terms of the transcription process with that mRNA. Therefore, the opposing strand of the DNA in the double helix is called the “antisense.” (Green Tr. at 103). Thus, when the DNA is wrapped together as a double helix, its sense and antisense strands essentially shut off the expression of the other, until the double helix opens up and the gene function again begins. (Green Tr. at 108) In artificially created antisense, the function of the DNA or RNA can be regulated by the introduction of a non-complementary strand. For example, mRNA can be manipulated through the introduction of an non-complementary RNA molecule. The non-complementary RNA would not make sense, and accordingly would shut off the function of the mRNA. (Green Tr. at 103). Antisense can also be introduced that attaches to the DNA sense strand, blocking the formation of the mRNA. (Green Tr. at 108). B. Antisense Experimentation in Dr. In-ouye’s Lab Dr. Inouye and his laboratory conducted experiments attempting to regulate gene expression by creating antisense constructs. (Green Tr. at 107). Dr. Pamela Green and Dr. Jack Coleman conducted many of the experiments in Dr. Inouye’s laboratory during this time. (Green Tr. at 116,188). The experiments in Dr. Inouye’s lab concentrated on three genes found in Escherichia coli (“E.coli ”), a prokaryotic bacterium. (Green Tr. at 108-09). These genes included the outer membrane protein A (“ompA”), the outer membrane protein C (“ompC”) and lipoprotein (“lpp”). (Green Tr. at 107). E. coli has been a model system for molecular experimentation since the 1940’s, used because it can be representative of the functions of larger, more complex organisms. (Green Tr. at 109-11). Moreover, basic principles discovered from experiments in E. coli can readily be extrapolated and applied to other organisms. (Green Tr. at 110). Dr. Inouye’s goal was to create antisense constructs which would shut off the expression of ompA, ompC and lpp. (Green Tr. at 114). To achieve this goal, a cloning vector was set up by inserting a promoter and terminator into a plasmid (a circular piece of DNA). The promoter facilitated the start of transcription and the terminator signaled the end. (Green Tr. at 114). Second, a segment of the target gene would be taken and flipped with respect to its usual orientation. (Green Tr. at 115,125). The promoter segment and termination segment would remain in ordinary position and order. (Green Tr. at 246). Third, the flipped gene segment would then be inserted in between the promoter and terminator of the cloning vector. (Green Tr. 115). Finally, the antisense construct would then be introduced into the E. coli bacteria through a method called transformation. (Green Tr. at 115). Dr. Inouye’s lab termed the antisense construct created by the flipped gene construct “messenger interfering complementary RNA” (“mieRNA”). (Green Tr. at 107, 115). Introduction of the mieRNA into the target cell had the expected result of stopping the function of the mRNA and shutting off the target gene that made the mRNA. (Green Tr. at 116). The mRNA, now bound to the mieRNA, could no longer function normally, because the mieRNA inhibited the expression of the gene. (PX 730, col. 3, lines 27-37). The experiments in Dr. Inouye’s lab were not without failures, however. Over a ten-year span, Dr. Inouye failed to regulate any other genes except for ompA, ompC and lpp, reporting ten or twelve failures in other E. coli genes, as well as yeast, oncogenes and eukaryotic cells. (Inouye Tr. at 357, 450-51, 458-460, 464-465). In addition, antisense regulation of the gene expression by mieR-NA in the ompA, ompC and lpp genes themselves was not always consistent, as introduction of antisense RNAs, intended to regulate the ompC gene, also shut off the function of the lpp gene, and vice versa. (Green Tr. at 117). Moreover, the success of the inhibition levels of the functions of the ompA, ompC and lpp genes often increased with the introduction of additional genes. (Green Tr. at 119). Dr. Inouye’s lab failed to regulate eukaryotic genes, including the SRV oncogene (Inouye Tr. at 458); the Kirsten oncogene (Inouye Tr. at 459) and thymidine ki-nase (Inouye Tr. at 460). However, at trial, Dr. Inouye explained that his laboratory failures in applying genetic antisense to other genes were just unsuccessful or incomplete experiments by graduate students with insufficient skill in the organism or gene sought to be regulated. (Inouye Tr. at 356-357, 464— 65, 492-93). Dr. Green testified at trial, and her laboratory notebooks confirmed that the date of conception of the antisense idea as developed in Dr. Inouye’s lab was June 3, 1983. The first step undertaken by Dr. Green in executing this idea occurred on August 26, 1983, and the first demonstration of antisense inhibition of ompA or ompC occurred sometime between August 26, 1983 and December 29, 1983. (Green Tr. at 211-12, 221). Dr. Inouye’s initial research efforts in the area of genetic antisense were first reported in an article published in the Japanese National Academy of Sciences in December, 1983. In the article, Dr. Inouye described natural antisense inhibition of ompF by micF RNA. (Inouye Tr. at 1475-76; PX 182). This article, published before his work in ompA, ompC and lpp, examined the proposition that micF RNA blocked translation of the ompF mRNA. (Falkinham Tr. at 1477-78). Dr. Inouye published the results of his laboratory’s work in ompA, ompC and lpp in Cell in June 1984. (Green Tr. at 120). He next coauthored a review article with Dr. Green in 1985 discussing the roles of anti-sense RNA that were available at that time in proka-ryotes and eukaryotes. (Green Tr. at 139; PX 344). C. Dr. Izant and Dr. Weintraub’s Work in Antisense Technology Dr. Izant and Dr. Weintraub also worked on artificial antisense to regulate the expression of a gene, but concentrated on eukaryotic genes instead of prokaryotic ones. Dr. Weintraub was a respected scientist, and a member of the Basic Sciences Division of the Fred Hutchinson Cancer Research Center. (Weintraub Dep. at 73; Reeder Tr. at 2055-56; Silverstein Tr. at 1317). Dr. Jonathan Izant was a post-doctoral fellow in Dr. Wein-traub’s laboratory from the middle of 1982 until 1986. (Izant Dep. at 14,15, 69). Dr. Weintraub and Dr. Izant conceived of the idea to regulate expression of TK genes in mouse cells by genetic antisense in 1982. In the spring of 1982, before Dr. Izant actually began working for Dr. Weintraub, they met and discussed the idea of inhibiting genes by introducing complementary nucleotide sequences which would bind with a target. (Weintraub Dep. at 302-05; Izant Dep. Vol. I at 18-19). In August of 1982, after arriving at Dr. Weintraub’s lab, Dr. Izant began experiments designed to regulate the expression of TK genes in mouse cells. (Izant Dep. Vol. I at 24-26; DX 82 (lab notebook)). Dr. Weintraub’s notebook indicates that between October 27, 1982 and November 1,1982 he was experimenting with the “reverse orientation of TK structural gene between its promoter and a poly-adeny-lation signal ... to produce antisense transcripts as potential anti-message.” (DX 82; Izant Dep. II at 21-33; (lab notebook)). Finally, in November of 1982, Dr. Izant began experimenting with a series of DNA constructs, including an antisense TK construct, and by December 13, 1982, he had made an antisense construct containing a promoter, a flipped HSV TK gene, and a polyadenylation signal. (Izant Dep. Vol. I at 44-45; DX 82 at 121 (lab notebook)). From November 1982 through 1983, Dr. Izant experimented with co-microinjections of sense and antisense TK genes into TK minus mouse cells. (Weintraub Dep. at 221, 277-80, 404-05). He also experimented with the idea of stably incorporating an antisense DNA into the cell’s DNA. (Izant Dep. Vol. I at 16; Weintraub Dep. at 167-70; DX 28 0Cell paper) at 1010, Table 2). Dr. Wein-traub also conducted experiments to confirm Dr. Izant’s initial successes. (Weintraub Dep. at 310-13; DX 39 (Science paper)). Both Dr. Izant and Dr. Weintraub reported rapid successes, with Dr. Izant first reporting inhibition of the TK gene as early as January 29,1983. (Izant Dep. Vol. II at 445-49; DX 82 at 147 (lab notebook)). Dr. Izant and Dr. Weintraub published the results of their antisense work in the April 1984 issue of the scientific journal Cell and the July 1985 issue of the scientific journal Nature. (Izant Dep. Vol. I at 16; Weintraub Dep. at 167-70; DX 28 (Cell paper) at 1010, Table 2). They also gave a presentation on their antisense work at the Gordon Conference on July 29, 1983. (Izant Dep. Vol. I at 67; Harland Dep. at 24-25). Moreover, they documented their successes in grant applications to the National Institute of Health (“NIH”) on January 5, 1983 and May 18, 1983. (Weintraub Dep. at 645-46; NIH grant application, DX 81 p. HW0182; DX 100 (letter to NIH)). They started work on their patent application in the fall of 1983, and filed the patent application in January of 1985. Dr. Izant and Dr. Weintraub became aware of Dr. Inouye’s work in antisense after their Cell paper was accepted for publication, but before it was actually published, which was sometime between December 1983 and April 1984. (Izant Dep. Vol. I at 196, 527-28; Weintraub Dep. at 193-95). Dr. Izant also become aware of advertisements published by Dr. Inouye in the November 17, 1983 issue of Nature magazine and the December 1983 issue of Cell. D. The Antisense Work of Other Scientists Many scientists who undertook research involving antisense technology experienced difficulty in achieving antisense in eukaryotic cells. (See, e.g., Wold Dep. at 84 (work in Thymidine kinase); Crowley Dep. at 54-55 (work in Dictyostelium discoideum — slime mold); Davis Dep. at 25-30 (work in saccha-romyces — baker’s yeast)). For example, Dr. Barbara Wold, an Enzo witness, testified at her deposition that there were many instances where antisense did not work to regulate the expression of a gene. (Wold Dep. at 84). Dr. Wold published an article in Cell with Dr. Stuart Kim, in which she postulated that a phenomena termed “posttranscriptional aberrant processing” existed in eukaryotic cells, but not prokaryotic cells. (Wold Dep. at 33-35, 49-51; see also Drs. Barbara Wold & Stuart Kim, Stable Reduction of Thymidine Kinase Activity in Cells Expressing High Levels of Antisense RNA, Cell, Vol. 42, pp. 129-38, Aug. 1985). Dr. Wold testified that to insure that antisense would work in a given gene would require experimentation on a case-by-case basis. (Wold Dep. at 50-51). Other scientists followed in the footsteps of Dr. Weintraub and Dr. Izant. For example, Dr. Weinberg, another consultant to Enzo, had attended the Weintraub presentation at the Gordon Conference. (Weinberg Dep. at 6-7; Weintraub Dep. at 203). His laboratory conducted experiments in September 1983 to inhibit an oncogene by antisense, which he described in his notebooks as the “Weintraub Experiment.” (Weinberg Dep. at 145). E. The Enzo Patent Prosecution 1. Patent Applications Dr. Inouye filed his original patent application for the ’931 Patent on October 20, 1983, disclosing only the example of natural anti-sense work with micF. (DX 3 at tab 1). He filed a second application on March 1, 1984, in which he disclosed his work with ompA, ompC and 1pp. (DX 5 at tab 1). The two patent applications were prosecuted separately until they were combined into a single application in 1989, which ultimately resulted in the issuance of the ’931 Patent. (DX 7 at tab 27). The only successful examples of antisense provided in the patent application were the work done by Dr. Green and Dr. Coleman in the ompA, ompC, and lpp genes, as well as the original work done by Dr. Inouye in the micF gene. (Green Tr. at 197, 230). Dr. Inouye later filed continuation and divisional applications which led to the issuance of the Enzo ’065 and ’149 Patents. 2. Prosecution History The PTO rejected Dr. Inouye’s patent applications ten times during prosecution on the grounds of non-enablement, citing its concerns that the technology was too unpredictable for application in other cells besides E. coli. The PTO also stated its belief that the contribution of the invention to the relevant technology was too small for such a broad protection of all genes in all cells. (See, e.g., Examiner’s Action to ’282, No. 585282, at 3-4 (Dec. 10, 1985); D.I. 218 at 223-250). Dr. Inouye responded to the PTO’s rejections by stating that the broad applicability of the invention to all genetic material had already been established, citing several articles that used artificial antisense to regulate organisms other than E. coli. (DX 5, tab 7 at 4-6). Neither Dr. Inouye nor Enzo disclosed to the PTO Dr. Inouye’s failures with regard to regulating other genes besides those disclosed, including other E. coli genes, as well as yeast and eukaryotic cells. In contrast, Dr. Inouye’s November 15, 1989 patent application claimed that his invention permitted anyone to construct an artificial mie system to regulate the expression of any specific gene in E. coli, including yeast. (In-ouye Tr. at 451; DX 7 at 598, tab 1 at 7, 8). Dr. Inouye and Enzo ultimately overcame the rejections of the PTO by filing the declaration of Dr. Saul Silverstein on October 2, 1990. (Hoscheit Tr. at 649; Joint Exh. 1C, tab 7A). Dr. Silverstein’s declaration asserted that Dr. Inouye’s invention was a general principle that could be applied without undue experimentation to all genes in all cells, and that it worked so well that no reference disclosed an inoperable application of anti-sense RNA. (Joint Exh. 1C, tab 7A at 14-15). 3.Dr. Inouye’s Actions During Prosecution In 1988, during the prosecution of the patents, Dr. Inouye published a review article in which he disclosed that his lab had failed to regulate the expression of other E. coli genes by antisense RNAs. (DX 13; Masayori In-ouye, Antisense RNA: its functions and applications in gene regulation — a review, at 30 (Nature, June 15, 1988); Tr. at 454-476). Moreover, he disclosed in this article that although successful reports existed on anti-sense RNA regulation in mammalian cells, there had been no successful report in yeast. Antisense RNA, supra, at 30. Dr. Inouye theorized that the reasons for the failures could be the instability of the individual RNAs of the individual cells, and concluded that it “remained to be seen how effectively the micRNA immune system could work in plants and animals”. Id. at 30, 32. In April of 1990, six months before the October 1990 patent application, Enzo sought federal funds from the NIH. The language of the NIH application asserted that “[d]espite ... considerable progress, there are no consistent ways in which to reliably generate an effective antisense gene for use in the inhibition of an endogenous or exogenous gene.” (Antisense Induction of Disease Resistance, Department of Health and Human Services, Small Business Innovation Research Program, Phase II Grant Application, at 18 (April 1, 1990); DX 148 at 18). However, at trial, Dr. Inouye testified that he had not disclosed this same opinion to the PTO. (In-ouye Tr. at 480). It is significant that in his initial application to the NIH, Dr. Inouye had sought over $700,000 to study whether anti-sense regulation would be successful in euka-ryotic cells. (See DX 69; Inouye Grant Application, at 48). F. The Calgene Patent Prosecution Calgene’s FLAVR SAVR tomato is unique in that it slows the ripening process of tomatoes on the vine by inhibiting the enzyme polygalacturonase (“PG”) through the use of antisense technology. (Knauf Tr. at 1859-60). Dr. Vic Knauf, a Calgene scientist, began research directed at applying antisense to plants in 1984 after hearing about the work of Dr. Weintraub. (Knauf Tr. at 1865, 1877). On December 12, 1985, Calgene scientists released a document in which they disclosed their antisense work in plants. (Knauf Tr. at 1879). Although Calgene initially considered plant antisense work to be a risky investment, Dr. Knauf and forty other scientists continued to work on it (Knauf Tr. at 1874, 1877), and by mid-to late-1986, the entire project pulled together. (Knauf Tr. at 1910). In 1988, Calgene’s scientists published a paper describing the inhibition of expression in plants through antisense. (Knauf-Tr. at 1892). Calgene invested approximately $20 million in research and development over a twelve year period to develop its FLAVR SAVR tomato. Calgene submitted its first patent application for its FLAVR SAVR tomato in September 1987, which was approved by the Patent and Trademark Office (“PTO”) on April 21,1992, resulting in the issuance of the Calgene ’065 Patent. (DX 2; PX 589). After the Calgene ’065 Patent issued, at least three different companies negotiated licenses with Calgene. (Knauf Tr. at 1864-65). G. Prior Litigation Between Enzo and Calgene During late 1992 and early 1993, Calgene was preparing for a public offering of its securities. (PX 664). During this period, Enzo released press statements on three different occasions announcing that Enzo was in the process of obtaining a broad antisense patent that would cover Calgene’s products. (Salquist Dep. at 22). Mr. Salquist, the Chief Executive Office of Calgene, testified that he believed the Enzo press releases were issued for the sole purpose of damaging Calgene. Id. Calgene offered expert testimony that Enzo’s actions adversely affected the sale price of its stocks. (Salquist Dep. at 123-124; Redington Dep. at 166, 177-78, 180-81; Ford Dep. at 17-18, 36, 43^14; Anderson Dep. at 7). In this regard, the witnesses testified that Calgene stock prices dropped from over $20 a share in the beginning of January 1993 to $15 by the end of January due to the activities of Enzo, including the press releases. (Salquist Dep. 135-136). In response to Enzo’s activities, on February 5, 1993, Calgene filed a lawsuit against Enzo in United States District Court in California, alleging interference with its stock price on four state law grounds. Calgene also sought a declaratory judgment to invalidate the Enzo ’931 Patent which had not yet issued. (DX 85). One month later, Enzo issued a press release announcing the issuance of its ’931 Patent for genetic antisense technology (PX 731), and on the following day, March 3, 1993, Enzo sued Calgene in this Court. (PX 723A). The district court in California dismissed Calgene’s declaratory judgment action in deference to the patent case pending in this Court, which Calgene unsuccessfully appealed. (DX 88 (Order after healing 6/21/93); PX 723A). Calgene then filed a motion to dismiss with prejudice the remaining claims in California, which was granted in August 1994. III. INFRINGEMENT Enzo claims that Calgene’s FLAVR SAVR tomato infringes both the Enzo ’931 and ’149 Patents. (D.I. 525 at 164). Calgene asserts that it has not infringed either patent. Although Enzo does not claim that Calgene infringes Enzo’s ’065 Patent, Calgene has counterclaimed for a declaratory judgment seeking a declaration that Calgene’s FLAVR SAVR tomato does not infringe Enzo’s ’065 Patent. (D.I. 54). A. Establishing an Infringement Claim A patent is infringed when a person “without authority makes, uses or sells any patented invention, within the United States during the term of the patent....” 35 U.S.C. § 271(a) (1995). The patent owner has the burden of proof, and must meet its burden by a preponderance of the evidence standard. SmithKline Diagnostics, Inc. v. Helena Lab. Corp., 859 F.2d 878, 889 (Fed.Cir.1988) (citations omitted). The preponderance of the evidence standard is met when a party provides evidence regarding a certain issue and that evidence is more convincing than the evidence offered in opposition to the issue. Hale v. Dep’t. of Transp., F.A.A., 772 F.2d 882, 885 (Fed.Cir.1985) (citations omitted). A patent owner may prove infringement under either of two theories: literal infringement or the doctrine of equivalents. Under the theory of literal infringement, infringement occurs where each element of at least one claim of the patent is found in the alleged infringer’s product. Panduit Corp. v. Dennison Mfg. Corp., 836 F.2d 1329, 1330 n. 1 (Fed.Cir.1987); Robert L. Harmon, Patents and the Federal Circuit 195 & n. 31 (3d ed.1994). A claim in a patent can only be infringed if it reads on each and every element of the alleged infringer’s product. American Hoist & Derrick Co. v. Manitowoc Co., Inc., 603 F.2d 629, 630 (7th Cir.1979); see also Amstar Corp. v. Envirotech Corp., 730 F.2d 1476, 1484 (Fed.Cir.1984), cert. denied, 469 U.S. 924, 105 S.Ct. 306, 83 L.Ed.2d 240 (1984) (infringement avoided only if element present in alleged infringing process absent in patented invention); Hormone Research Found., Inc. v. Genentech, 904 F.2d 1558, 1562 (Fed.Cir.1990), cert. dismissed, 499 U.S. 955, 111 S.Ct. 1434, 113 L.Ed.2d 485 (1991) (infringement only if each claim or equivalent found in accused invention). If a patent has a series of claims, and one claim is infringed, then the entire patent is infringed. Panduit, 836 F.2d at 1330 n. 1. Under the theory of the doctrine of equivalents, however, infringement may be established even where elements in the claimed invention are missing from the alleged infringer’s product, if the “accused device performs substantially the same function in substantially the same way to achieve substantially the same result as the claimed device.” Graver Tank & Mfg. Co. v. Linde Air. Prods. Co., 339 U.S. 605, 608, 70 S.Ct. 854, 94 L.Ed. 1097 (1950); Warner-Jenkinson Company, Inc. v. Hilton Davis Chemical Co., 520 U.S, 17, 117 S.Ct. 1040, 137 L.Ed.2d 146 (1997) (declining to overrule Graver Tank); Malta v. Schulmerich Carillons, Inc., 952 F.2d 1320, 1325 (Fed.Cir.1991). To find infringement under either theory, the Court must undertake a two-step process. First, it must interpret the claims at issue by evaluating the language of the claims (“claim interpretation”). Miles Lab., Inc. v. Shandon, Inc., 997 F.2d 870, 876 (Fed.Cir.1993), cert. denied, 510 U.S. 1100, 114 S.Ct. 943, 127 L.Ed.2d 232 (1994). Claim interpretation is a question of law. Markman v. Westview Instruments, Inc., 52 F.3d 967, 977-978 (Fed.Cir.1995), aff'd, 517 U.S. 370, 388-390, 116 S.Ct. 1384, 134 L.Ed.2d 577 (1996). When construing the claims of a patent, a court considers the literal language of the claim, the patent specification and the prosecution history. Markman, 52 F.3d at 978. A court may consider extrinsic evidence, including expert and inventor testimony, dictionaries, and learned treatises, in order to assist it in construing the true meaning of the language used in the patent. Id. at 980 (citations omitted). A court should interpret the language in a claim by applying the ordinary and accustomed meaning of the words in the claim. Envirotech Corp. v. Al George, Inc., 730 F.2d 753, 759 (Fed.Cir.1984). However, if the patent inventor clearly supplies a different meaning, the claim should be interpreted accordingly. Markman, 52 F.3d at 980 (noting that pat-entee is free to be his own lexicographer, but emphasizing that any special definitions given to words must be clearly set forth in patent). If possible, claims should be construed to uphold validity. In re Yamamoto, 740 F.2d 1569, 1571 & n. * (Fed.Cir.1984) (citations omitted). The second step to determine infringement requires a court to compare the accused products or patented claims with the properly construed claims of the patent at issue to determine whether the accused products or processes infringe on the patent under either the theory of literal infringement or under the theory of the doctrine of equivalents (“infringement analysis”). Miles Lab., 997 F.2d at 876; SRI Int’l v. Matsushita Elec. Corp. of America, 775 F.2d 1107, 1121 (Fed.Cir.1985). B. The ’931 Patent Enzo alleges that Calgene’s FLAVR SAVR tomato literally infringes Claims 1, 3, 5, 7, 34, 66, 73 and 74 of the ’931 Patent. (D.I. 525 at 164). To determine whether the Calgene FLAVR SAVR tomato infringes the Enzo ’931 Patents, the Court will first construe the claims to determine their meaning, and will then compare the FLAVR SAVR tomato to the claims of the ’931 Patent. 1. Claim interpretation a. Claim 1 of the ’931 Patent Claim 1 of the ’931 Patent teaches the underlying invention of antisense common to each Enzo patent. It provides: A prokaryotic or eukaryotic cell containing a nonnative DNA construct, which construct produces an RNA which regulates the function of a gene, said DNA construct containing the following operably linked DNA segments: (a) A transcriptional promoter segment; (b) A transcription termination segment; (c) A DNA segment; whereby transcription of the DNA segment produces a ribonucleotide sequence which does not naturally occur in the cell, is complementary to a ribonucleotide sequence transcribed from said gene, and said nonnaturally occurring ribonucleotide sequence regulates the function of said gene. (1) A prokaryotic or eukaryotic cell... The Court concludes that the first element of claim 1 of the ’931 Patent applies to both prokaryotic and eukaryotic cells by virtue of the presence of the word “or.” (2) Containing a nonnative DNA construct. .. The Court concludes that the pro-karyotic or eukaryotic cell referred to in the first element must contain a DNA construct. This DNA construct must be comprised of a small DNA fragment or segment containing the promoter, the terminator and the genetic sequence in between as more fully described in elements (4)-(7). In addition, the Court construes the term “nonnative” to mean that the DNA construct must not occur naturally in the cell, but instead must be introduced into the cell from an outside source. (3) Which construct produces an RNA which regulates the function of a gene... The Court concludes that the nonnative DNA construct must carry out normal cellular functions, including transcription and translation. Thus, upon transcription, the DNA construct must split its double helix, an RNA polymerase must then synthesize with one of the DNA strands according to base-pairing rules, and the RNA polymerase ultimately must produce an mRNA. Finally, the Court concludes that this non-naturally occurring mRNA must “regulate the function of a gene” by binding with a naturally-occurring mRNA from the gene targeted, and preventing the naturally-occurring mRNA from functioning. (4) Said DNA construct containing the following operably linked DNA segments ... The Court construes the term “[sjaid DNA construct” to mean the nonnative DNA construct as interpreted in element (2). The term “operably linked” means that the segments must function together as they are attached to create the DNA construct. (5) A transcriptional promoter segment. .. The Court concludes that the promoter is the portion of the DNA construct which facilitates the start of the transcription of the RNA. (Green Tr. at 114). This promoter must be the starting point for the RNA polymerase to begin reading the information necessary for transcription. (Falkin-ham Tr. at 1413). (6) A transcription termination segment. .. The Court interprets the term “transcription termination segment” to mean a configuration of bases on the fragment of the DNA construct, which must signal the end point of the RNA molecule. (Green Tr. at 114; Falkinham Tr. at 1412). Accordingly, the genetic message must “stop” at the terminator sequence or segment. (Falkin-ham Tr. at 1414). (7) And therebetween, a DNA segment ... The Court construes this element to require that the nonnative DNA construct must contain a DNA segment between the transcriptional promoter segment and the transcription termination segment. (8) Whereby transcription of the DNA segment produces a ribonucleotide sequence ... The Court concludes that during transcription of the nonnative DNA segment, its double helix must separate and the RNA polymerase must produce an mRNA. This mRNA must be a single stranded ribonucleo-tide sequence complementary to the DNA from which it was produced. (9) Which does not naturally occur in the cell... The Court construes element (9) to require that the RNA sequence described in element (8) must result from the introduction of nonnative DNA construct into the cell. In other words, the cell must not be able to produce the RNA sequence on its own. (10) Is complementary to a ribonucleo-tide sequence transcribed from said gene... The Court concludes that the non-naturally occurring RNA sequence described in elements (8) and (9) must be complementary to a naturally occurring RNA sequence produced by the gene. However, necessary to a complete construction of this claim is the meaning of the term “complementary,” which is disputed by the parties. Enzo claims that the specification of the ’931 Patent defines the term “complementary” as “capable of hybridizing.” For example, in column 2, lines 63-66 of the ’931 Patent, it states that the DNA construct is “transcribed to produce an mRNA (micRNA) which is complementary to and capable of binding or hybridizing with the mRNA transcribed by the gene to be regulated.” In interpreting a patent claim, a court generally gives the words in a claim their ordinary and customary meaning. Vitronics Corp. v. Conceptronic, Inc., 90 F.3d 1576, 1582 (Fed.Cir.1996). However, “a pat-entee may be his [or her] own lexicographer and use terms in a manner other than their ordinary meaning, as long as the special definition of the term is clearly stated in the patent specification or file history.” Id. (citations omitted) (emphasis added). In reviewing the patent specification in this case, the Court concludes that the specification fails to clearly define the term “complementary.” It is the Court’s view that the use of the word “and” in the specification’s references to the term “complementary” and the phrase “capable of hybridization” suggest that the specification is referring to two different characteristics of the RNA. While complementarity may be necessary for hybridization, the Court is not persuaded that the concepts are synonymous, such that one term defines the other. Accordingly, the Court rejects Enzo’s contention that the patent defines the term “complementary.” Because the Court concludes that the term “complementary” is not given a special meaning in the ’931 Patent, the Court must turn to the ordinary and customary meaning of the term. Ordinarily defined in the context of genetic technology, the term “complementary” means “... the capacity for the precise pairing of ... bases between strands of DNA and sometimes RNA such that the structure of one strand determines the other.” Webster’s Ninth Collegiate Dictionary 269 (1983) (emphasis added). Relying in part on this definition, Calgene contends that the term complementary should be narrowly construed to require complete complementarity. In response, Enzo maintains that complementary means “capable of hybridizing” and that there are no degrees or percentages of complementarity. Based on the record in this case, including the testimony of Dr. Knauf, which the Court finds credible, the Court rejects Enzo’s argument and concludes that an appropriate definition of the term “complementary” requires quantification. To the extent that Enzo’s definition of complementary as “capable of hybridizing” suggests that the ’931 Patent permits any degree of complementarity, the Court rejects Enzo’s contention as contrary to the evidence and to existing precedent. Every example of operable antisense constructs in the specification of the ’931 Patent involves a gene, or a portion of a gene, which is removed and inverted in the opposite orientation in a plasmid, and which thus, has complete complementarity with a single segment of the transcribed RNA. Indeed, because there are only four nucleotides which make up RNA, every RNA strand will have individual nucleotides and short sequences of nucleotides which are complementary to another RNA and thus, there would always be a theoretical possibility of hybridization. However, if this were the case, and the Court were to accept Enzo’s contention that complementary means “capable of hybridizing,” and as such, any degree of complementarity is sufficient under the ’931 Patent, then the “complementary” limitation would be meaningless. In addition, the Court finds this issue to be analogous to the issue before the Court of Appeals for the Federal Circuit in Genentech, Inc. v. Wellcome Found. Ltd., 29 F.3d 1555 (Fed.Cir.1994). In Genentech, the phrase at issue was “human tissue plasmino-gen activator” (“t-PA”). In interpreting this phrase, the Court rejected the broad definition sought by the patentee, which would include proteins whose amino acid sequences were not identical to natural t-PA, so long as they included important segments of the sequence or were capable of serving the same function as natural t-PA. In rejecting this broad definition, the Federal Circuit noted that the definition would cover “an infinite number of permutations,” many of which would be inoperable, and that there was “no basis provided in the specification for determining which of these permutations are operative and which are not.” Id. at 1564 (citing Amgen Inc. v. Chugai Pharmaceutical Co. Ltd., 927 F.2d 1200, 1212-14 (Fed.Cir.1991)). Similarly, in this case, the Court notes that the specification for the ’931 Patent provides no guidance for determining when less than complete complementarity would make an operable antisense construct. Moreover, as discussed earlier, the specification only provides examples of operable antisense constructs that had complete complementarity with a single segment of transcribed RNA. Following the Genentech decision, the Court will reject the broad definition Enzo seeks, because the specification provides no basis for determining when less than complete complementarity would be successful. The Court concludes that this element of the claim requires the bases of the two ENA strands to precisely or exactly pair together according to the base pairing rules for ENA, such that complete complementarity exists between the two strands. Also of importance to the interpretation of this claim is the meaning of the phrase “said gene” in element (10). In interpreting this language, the Court construes element (10) to require that the complementary ENA sequence must be transcribed from the gene described in element (3). (11) Said nonnaturally occurring ribo-nucleotide sequence regulates the function of said gene ... The Court construes element (11) to require that the non-naturally occurring ENA sequence described in elements (8), (9), and (10) must produce an mENA, which must be complementary to and pair with the naturally-occurring mENA produced by ENA which is produced by the gene. The Court concludes further that this non-naturally occurring mENA sequence must “regulate the function” of the gene by binding to the naturally-occurring mENA and preventing it from functioning. In other words, the function of the naturally-occurring mENA must be inhibited or disabled by the introduction of the non-naturally occurring mENA sequence. b. Claim 3 of the ’931 Patent. Claim 3 provides: A method of regulating the function of a gene in a prokaryotic and eukaryotic cell which comprises introducing into said cell the DNA construct of claim 1. The Court concludes that Claim 3 is a method claim, and identifies the method of regulating gene function utilizing the construct as interpreted in Claim 1. Accordingly, Claim 3 has no additional elements that the Court must interpret. c. Claim 5 of the ’931 Patent. Claim 5 of the ’931 Patent teaches regulation of the gene function by use of an inverted gene segment. Claim 5 reads as follows: A nonnative DNA construct which when present in a prokaryotic or eukaryotic cell containing a gene produces an ENA which regulates the function of said gene, said DNA construct containing the following operably linked DNA segments: a. A transcriptional promoter segment; b. A transcription termination segment; c. A DNA segment comprising a segment of said gene, said gene segment located between said promoter segment and said termination segment and being inverted with respect to said promoter segment and said termination segment whereby the ENA produced by transcription of the inverted gene segment regulates the function of said gene. (1) A nonnative DNA construct ... The Court concludes that interpretation of this element does not differ from element (2) of Claim 1 of the ’931 Patent. (2) Which when present in a prokaryotic or eukaryotic cell containing a gene ... The Court concludes that, like element (1) of Claim 1, this element teaches both proka-ryotic and eukaryotic cells. In this element, however, the cell must contain a gene. (3) Which regulates the function of said gene ... (4) Said DNA construct containing the following operably linked DNA segments (5) a transcriptional promoter segment (6) a transcription termination segment; and ... The Court concludes that interpretation of these four elements of Claim 5 do not differ from elements (3)-(7) of Claim 1 of the ’931 Patent. (7) a DNA segment comprising a segment of said gene ... The Court construes this element to require that the nonnative DNA construct must contain a DNA segment which includes a portion of the targeted gene. (8) Said gene segment located between said promoter segment and said termination segment ... The Court construes this element to mean that the segment of the target gene taught in element (7) must be situated between the transcriptional promoter segment and the transcription terminator segment of the DNA construct. (9) And being inverted with respect to said promoter segment and said termination segment ... The Court concludes that this element requires an inverted gene segment, or, in other words, a “flipped” gene, or a gene that is placed in reverse orientation to the transcriptional promoter and transcription termination segments. The promoter and termination segments, however, must remain in ordinary position and order. (10) Whereby the RNA produced by transcription of the inverted gene segment regulates the function of said gene ... The Court concludes that, like element (11) of Claim 1 of the ’931 Patent, this claim teaches that the mRNA produced by transcription of the non-naturally occurring DNA must bind to the naturally-occurring mRNA, preventing the native mRNA from functioning. However, unlike element (11) of the ’931 Patent, this claim requires that a flipped gene sequence described in element (9) must produce the mRNA that ultimately regulates the function of the gene. d. Claim 7 of the ’931 Patent. Claim 7 provides: A method of regulating the function of a gene in a prokaryotic or eukaryotic cell which comprises introducing into said cell the DNA construct of claim 5. The Court construes Claim 7 as a method claim directed to the method of regulating gene function utilizing the construct as interpreted in Claim 5, and which needs no further interpretation. e. Claim 34 of the ’931 Patent. Claim 34 provides: A nonnative nucleotide construct which, when present in a cell containing a gene, produces an RNA which regulates the function of said gene, said polynucleotide construct containing the following opera-tively linked polynucleotide segments: a. a transcriptional promoter segment; b. a transcription termination segment; and there between; c. a polynucleotide segment; where by transcription of a polynucleotide segment produces a ribonucleotide sequence which does not naturally occur in the cell, is complementary to a ribonucleo-tide sequence transcribed from said gene, and said non-naturally occurring ribonu-cleotide sequence regulates the function of said gene. The Court construes the elements of Claim 34 to be no different from the elements in Claim 1 of the ’931 Patent except that the fourth element of this claim teaches a “poly-nucleotide construct,” whereas Claim 1 teaches a DNA construct. The Court concludes that a “polynucleotide construct” is a “cellular constituent that is one of the building blocks of ribonucleic acids (RNA) and deoxyribonucleic acid (DNA). In biological systems, nucleotides are linked by enzymes in order to make long, chain like polynucleotide of defined sequence.” 12 McGraw-Hill Encyclopedia of Science and Technology 235 (7th ed.1992). DNA is only one example of a polynucleotide construct in which nucleic acids are strung together in a certain configuration. (Green Tr. at 94; Fal-kinham Tr. at 1426; Shewmaker Dep. at 61). Therefore, the Court concludes that this claim teaches any polynucleotide construct, not just DNA. f. Claim 66 of the ’931 Patent. Claim 66 provides: A method of regulating a function of a gene in a cell which comprises introducing into said cell the polynucleotide construct of ... claim 34_ The Court concludes that Claim 66 is a method claim directed to the method of regulating the gene function utilizing the polynu-cleotide sequence as interpreted in Claim 34, and needs no further interpretation. g. Claim 73 of the ’931 Patent. Claim 73 provides: A cell containing a nonnative polynucleo-tide construct, which construct produces an RNA which regulates the function of a gene, said polynucleotide construct containing the following operably linked poly-nucleotide segments: a. a transcriptional promoter segment: b. a transcription termination segment; c. a polynucleotide segment comprising a segment of said gene, said gene segment located between said promoter segment and said termination segment and being inverted with respect to said promoter segment and said termination segment, whereby the RNA produced by transcription of the inverted gene segment regulates the function of said gene. The Court concludes that the elements of Claim 73 are identical to Claim 5, except that Claim 73 teaches a nonnative polynucleotide rather than a nonnative DNA construct. As interpreted in Claim 34 of the '931 Patent, a DNA construct is an example of a polynu-cleotide sequence, and the Court accordingly construes this claim to be directed to all polynucleotide sequences, not just DNA. h. Claim 74 of the ’931 Patent. Claim 74 provides: “The cell of claim 73 wherein said cell is prokaryotic.” The Court concludes that Claim 74 is a dependent claim on Claim 73. The claim requires that the cell referred to in Claim 73 must be a prokaryotic cell, which does not contain a nucleus or a nuclear membrane. 2. Literal Infringement of Enzo’ 931 Patent Having interpreted the claims of the ’931 Patent, the Court will now compare the meaning of these claims to the elements found in the FLAVR SAVR tomato, as required in a literal infringement analysis. a. Claim 1 of the ’931 Patent. (1)A prokaryotic or eukaryotic cell ... The Court finds that the FLAVR SAVR tomato contains eukaryotic cells. The Court has construed element one to teach both prokaryotic and eukaryotic cells, and accordingly, element (1) is present in the FLAVR SAVR tomato. (2) Containing a nonnative DNA construct ... The Court finds that the FLAVR SAVR tomato utilizes an antisense construct comprised of a nonnative DNA plasmid which combines the promoter and termination segments and the genetic sequence in between. (Knauf Tr. at 1967-68). The Court has construed element (2) of the ’931 Patent to require a small DNA fragment or segment that does not occur naturally in the cell, and which contains the promoter, the terminator and the genetic sequence in between. These elements are more fully discussed in elements (4) — (7). The Court finds that element (2) is present in the FLAVR SAVR tomato. (3) Which construct produces an RNA which regulates the function of a gene ... The Court finds that once the FLAVR SAVR nonnative DNA construct, as defined in element (2), is inserted into the eukaryotic cell, it carries out normal cellular functions, such as transcription and translation. The construct produces an mRNA through transcription (Sheehy Dep. at 13-14), which is then translated to achieve polygalacturonase, or the PG enzyme. (Knauf Dep. at 151). The PG antisense construct is complementary to the PG mRNA, and shuts off the function of the PG mRNA, ultimately affecting the expression of the PG gene. (Knauf Dep. at 152-53). The Court has construed element (3) of Claim 1 to require that the nonnative DNA construct must carry out normal cellular functions, including transcription and translation, and that the resulting non-naturally occurring mRNA must “regulate the function of a gene” by binding with a naturally-occurring mRNA from the gene targeted, and preventing the naturally-occurring mRNA from functioning. The Court finds element (3) is present in the FLAVR SAVR tomato. (4) Said DNA construct containing the foll