Multicellular living organisms and unmodified parts thereof and – Method of introducing a polynucleotide molecule into or... – The polynucleotide confers pathogen or pest resistance
Patent
1997-12-09
2000-08-08
Smith, Lynette R. F.
Multicellular living organisms and unmodified parts thereof and
Method of introducing a polynucleotide molecule into or...
The polynucleotide confers pathogen or pest resistance
435 691, 435 701, 435440, 435468, 435469, 435474, 435410, 435419, 4353201, 536 231, 536 236, 536 233, 800278, 800290, 8003174, C12N 1529, C12N 504, C12N 1582, A01H 500
Patent
active
061004499
DESCRIPTION:
BRIEF SUMMARY
FIELD OF THE INVENTION
The present invention relates to genes from the I2 Fusarium resistance locus of tomato belonging to a multigene family herein designated I2C, useful either as a tomato resistance gene to plant vascular diseases caused by Fusarium pathogens, or as probes for breeding Fusarium resistant tomatoes or for screening of new diseases in related plants of the Solanaceae family, and to transformed plants, particularly Fusarium resistant tomatoes.
BACKGROUND OF THE INVENTION
Resistance to pathogens is thought to involve a specific recognition between a resistant plant and the pathogen, which triggers a set of responses that act to confine the pathogen. The specificity of this process is considered to involve a recognition between the products of a plant resistance (R) gene and a cognate pathogen avirulence gene (Dangl, 1995; Staskawicz et al., 1995). The characterization of resistance genes is of major importance for elucidating the initiation of the cascade of events that leads to specific resistance responses, as well as for more efficient introduction of resistance to pathogens into important crops.
Several resistance genes have been cloned recently by positional cloning or by transposon tagging. These genes include: the HM1 gene of maize (Johal and Briggs, 1992), the Pto gene of tomato (Martin et al., 1993), the Cf-9 gene of tomato (Jones et al., 1994), the RPS2 (Bent et al., 1994; Mindrinos et al., 1994) and the RPM1 (Grant, 1995) genes from Arabidopsis, the N gene from tobacco (Whitham et al., 1994), and the L6 gene from flax (Ellis et al., 1995; Lawrence et al, 1995). These resistance genes show diverse biological characteristics. The HM1 gene is the only example to date where the gene product acts directly to inactivate a component of the pathogen attack, or a compatibility factor (Briggs and Johal, 1994). The other genes belong to a different genetic category, that of incompatibility (or gene for gene) interaction, based on the recognition by the resistance gene product of in avirulence (or incompatibility) component of the pathogen, which does not necessarily participate in the compatibility or in the infection processes (Briggs and Johal, 1994). These genes are all involved in resistance processes characterized by hypersensitive response (HR). In spite of their origin from different plant species, and their divergent specificity to viral, fungal or bacterial pathogens, a group of these R genes share several structural features. A nucleotide-binding domain (P-loop) and five additional amino-acid stretches of unknown function are conserved in their N-terminal region. A region of leucine-rich repeats (LRR) is present in their C terminus, though the consensus sequence and the length of the repeats are different among them. LRR were shown to be involved in protein-protein interactions in other proteins (Kobe and Deisenhofer, 1994; Kobe and Deisenhofer, 1995), and may have similar role in resistance genes. The N gene, the L6 gene and the Cf-9 gene were shown to belong to large gene families, partially clustered with the resistance gene. The detailed genomic distribution of these multigene families is yet unknown.
The soil-born fungus Fusarium oxysporum is the causative agent of severe will diseases in a large variety of plant species world-wide. It is an imperfect fungus for which no sexual cycle is known. The tomato-specific pathogen Fusarium oxysporum f. sp. lycopersici (F.o.l) causes the disease Fusarium wilt. The fungus penetrates the vascular system of roots from both resistant and susceptible varieties, mainly through wounds. During a compatible interaction, which leads to disease, the fungus proceeds through the vascular system which eventually collapses. This leads to wilt and often to death of the plant. During an incompatible interaction, resulting in resistance, the fungus is confined to the lower part of the roots, and further symptoms do not develop. Several mechanisms, not including HR, were suggested to be involved in this resistance. They include: the production of inhi
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Eshed Yuval
Fluhr Robert
Ori Naomi
Paran Ilan
Zamir Daniel
Smith Lynette R. F.
Yeda Research and Development Co. Ltd.
Yissum Research and Development Company
Zaghmout Ohsama M-Faiz
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