Multicellular living organisms and unmodified parts thereof and – Plant – seedling – plant seed – or plant part – per se – Higher plant – seedling – plant seed – or plant part
Reexamination Certificate
1997-12-03
2001-05-22
Hutzell, Paula (Department: 1638)
Multicellular living organisms and unmodified parts thereof and
Plant, seedling, plant seed, or plant part, per se
Higher plant, seedling, plant seed, or plant part
C514S002600, C514S012200, C800S298000, C800S305000, C800S306000, C800S307000, C800S308000, C800S309000, C800S310000, C800S311000, C800S312000, C800S313000, C800S314000, C800S315000, C800S317000, C800S317100, C800S317200, C800S317300, C800S317400, C800S318000, C800S319000, C800S320000, C800S320100, C800S320200
Reexamination Certificate
active
06235974
ABSTRACT:
FIELD OF THE INVENTION
The present invention relates to imparting hypersensitive response induced resistance to plants by treatment of seeds.
BACKGROUND OF THE INVENTION
Living organisms have evolved a complex array of biochemical pathways that enable them to recognize and respond to signals from the environment. These pathways include receptor organs, hormones, second messengers, and enzymatic modifications. At present, little is known about the signal transduction pathways that are activated during a plant's response to attack by a pathogen, although this knowledge is central to an understanding of disease susceptibility and resistance. A common form of plant resistance is the restriction of pathogen proliferation to a small zone surrounding the site of infection. In many cases, this restriction is accompanied by localized death (i.e., necrosis) of host tissues. Together, pathogen restriction and local tissue necrosis characterize the hypersensitive response. In addition to local defense responses, many plants respond to infection by activating defenses in uninfected parts of the plant. As a result, the entire plant is more resistant to a secondary infection. This systemic acquired resistance can persist for several weeks or more (R. E. F. Matthews,
Plant Virology
(Academic Press, New York, ed. 2, 1981)) and often confers cross-resistance to unrelated pathogens (J. Kuc, in
Innovative Approaches to Plant Disease Control
, I. Chet, Ed. (Wiley, New York, 1987), pp. 255-274, which is hereby incorporated by reference). See also Kessman, et al., “Induction of Systemic Acquired Disease Resistance in Plants By Chemicals,”
Ann. Rev. Phytopathol
. 32:439-59 (1994), Ryals, et al., “Systemic Acquired Resistance,”
The Plant Cell
8:1809-19 (Oct. 1996), and Neuenschwander, et al., “Systemic Acquired Resistance,”
Plant
-
Microbe Interactions
vol. 1, G. Stacey, et al. ed. pp. 81-106 (1996), which are hereby incorporated by reference.
Expression of systemic acquired resistance is associated with the failure of normally virulent pathogens to ingress the immunized tissue (Kuc, J., “Induced Immunity to Plant Disease,”
Bioscience
, 32:854-856 (1982), which is hereby incorporated by reference). Establishment of systemic acquired resistance is correlated with systemic increases in cell wall hydroxyproline levels and peroxidase activity (Smith, J. A., et al., “Comparative Study of Acidic Peroxidases Associated with Induced Resistance in Cucumber, Muskmelon and Watermelon,”
Physiol. Mol. Plant Pathol
. 14:329-338 (1988), which is hereby incorporated by reference) and with the expression of a set of nine families of so-called systemic acquired resistance gene (Ward, E. R., et al., “Coordinate Gene Activity in Response to Agents that Induce Systemic Acquired Resistance,”
Plant Cell
3:49-59 (1991), which is hereby incorporated by reference). Five of these defense gene families encode pathogenesis-related proteins whose physiological functions have not been established. However, some of these proteins have antifungal activity in vitro (Bol, J. F., et al., “Plant Pathogenesis-Related Proteins Induced by Virus Infection,”
Ann. Rev. Phytopathol
. 28:113-38 (1990), which is hereby incorporated by reference) and the constitutive expression of a bean chitinase gene in transgenic tobacco protects against infection by the fungus
Rhizoctonia solani
(Broglie, K., et al., “Transgenic Plants with Enhanced Resistance to the Fungal Pathogen Rhizoctonia Solani,”
Science
254:1194-1197 (1991), which is hereby incorporated by reference), suggesting that these systemic acquired resistance proteins may contribute to the immunized state (Uknes, S., et al., “Acquired Resistance in Arabidopsis,”
Plant Cell
4:645-656 (1992), which is hereby incorporated by reference).
Salicylic acid appears to play a signal function in the induction of systemic acquired resistance since endogenous levels increase after immunization (Malamy, J., et al., “Salicylic Acid: A Likely Endogenous Signal in the Resistance Response of Tobacco to Viral Infection,”
Science
250:1002-1004 (1990), which is hereby incorporated by reference) and exogenous salicylate induces systemic acquired resistance genes (Yalpani, N., et al., “Salicylic Acid is a Systemic Signal and an Inducer of Pathogenesis-Related Proteins in Virus-Infected Tobacco,”
Plant Cell
3:809-818 (1991), which is hereby incorporated by reference), and acquired resistance (Uknes, S., et al., “Acquired Resistance in Arabidopsis,”
Plant Cell
4:645-656 (1992), which is hereby incorporated by reference). Moreover, transgenic tobacco plants in which salicylate is destroyed by the action of a bacterial transgene encoding salicylate hydroxylase do not exhibit systemic acquired resistance (Gaffney, T., et al., “Requirement of Salicylic Acid for the Induction of Systemic Acquired Resistance,”
Science
261:754-56 (1993), which is hereby incorporated by reference). However, this effect may reflect inhibition of a local rather than a systemic signal function, and detailed kinetic analysis of signal transmission in cucumber suggests that salicylate may not be essential for long-distance signaling (Rasmussen, J. B., et al., “Systemic Induction of Salicylic Acid Accumulation in Cucumber after Inoculation with
Pseudomonas Syringae
pv.
Syringae,” Plant Physiol
. 97:1342-1347) (1991), which is hereby incorporated by reference).
Immunization using biotic agents has been extensively studied. Green beans were systemically immunized against disease caused by cultivar-pathogenic races of
Colletotrichum lindemuthianum
by prior infection with either cultivar-nonpathogenic races (Rahe, J. E., “Induced Resistance in
Phaseolus Vulgaris
to Bean Anthracnose,”
Phytopathology
59:1641-5 (1969); Elliston, J., et al., “Induced Resistance to Anthracnose at a Distance from the Site of the Inducing Interaction,”
Phytopathology
61:1110-12 (1971); Skipp, R., et al., “Studies on Cross Protection in the Anthracnose Disease of Bean,”
Physiological Plant Pathology
3:299-313 (1973), which are hereby incorporated by reference), cultivar-pathogenic races attenuated by heat in host tissue prior to symptom appearance (Rahe, J. E., et al., “Metabolic Nature of the Infection-Limiting Effect of Heat on Bean Anthracnose,”
Phytopathology
60:1005-9 (1970), which is hereby incorporated by reference) or nonpathogens of bean. The anthracnose pathogen of cucumber,
Colletotrichum lagenarium
, was equally effective as non-pathogenic races as an inducer of systemic protection against all races of bean anthracnose. Protection was induced by
C. lagenarium
in cultivars resistant to one or more races of
C. lindemuthianum
as well as in cultivars susceptible to all reported races of the fungus and which accordingly had been referred to as ‘lacking genetic resistance’ to the pathogen (Elliston, J., et al., “Protection of Bean Against Anthracnose by Colletotrichum Species Nonpathogenic on Bean,”
Phytopathologische Zeitschrift
86:117-26 (1976); Elliston, J., et al., “A Comparative Study on the Development of Compatible, Incompatible and Induced Incompatible Interactions Between Collectotrichum Species and
Phaseolus Vulgaris,” Phytopathologische Zeitschrift
87:289-303 (1976), which are hereby incorporated by reference). These results suggest that the same mechanisms may be induced in cultivars reported as ‘possessing’ or ‘lacking’ resistance genes (Elliston, J., et al., “Relation of Phytoalexin Accumulation to Local and Systemic Protection of Bean Against Anthracnose,”
Phytopathologische Zeitschrift
88:114-30 (1977), which is hereby incorporated by reference). It also is apparent that cultivars susceptible to all races of
C. lindemuthianum
do not lack genes for induction of resistance mechanisms against the pathogen.
Kuc, J., et al., “Protection of Cucumber Against
Collectotrichum Lagenarium
by
Colletotrichum Lagenarium,” Physiological Plant Pathology
7:195-9 (1975), which is hereby incorporated by reference), showed that cucumber plants could be systemically protected against disease caused by
Colletotr
Beer Steven V.
Qiu Dewen
Wei Zhong-Min
Cornell Research Foundation Inc.
Hutzell Paula
Nixon & Peabody LLP
Zaghmout Ousama M-Faiz
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