PAD4 nucleic acid compositions from Arabidopsis and methods...

Details PAD4 nucleic acid compositions from Arabidopsis and methods... PAD4 nucleic acid compositions from Arabidopsis and methods...

1999-11-04

2003-09-16

Nelson, Amy J. (Department: 1638)

Multicellular living organisms and unmodified parts thereof and

Method of introducing a polynucleotide molecule into or...

C435S320100, C435S419000, C536S023600

Reexamination Certificate

active

06620985

ABSTRACT:

FIELD OF THE INVENTION
The present invention relates to compositions obtainable from plants, and methods for enhancing disease resistance of plants using the compositions. More particularly, the invention relates to nucleic acid compositions and encoded polypeptides, as well as microorganisms and plants transformed with the nucleic acid for production of encoded polypeptides.
BACKGROUND OF THE INVENTION
When a plant pathogen interacts with a potential host, it may successfully colonize the host and cause disease, in which case the pathogen is said to be virulent, the host is susceptible, and the interaction is compatible. Alternatively, the plant may respond to the pathogen by rapidly activating a battery of defense responses, interfering with pathogen multiplication and preventing disease. In this case, the pathogen is said to be avirulent, the host is resistant, and the interaction is incompatible. The outcomes of plant-pathogen interactions often fit a “gene-for-gene” model. In this model, resistance results when the pathogen carries a particular avirulence gene that corresponds to a particular resistance gene (R gene) in the host. In general, each R gene confers resistance only to pathogens carrying the corresponding avirulence gene. Gene-for-gene resistance responses have been observed in interactions of plants with a wide variety of pathogens, including fungi, bacteria and viruses. A simple molecular explanation for gene-for-gene resistance is that avirulence genes encode ligands that bind to receptors encoded by the plant R genes or that avirulence gene products synthesize such ligands. Ligand binding triggers activation of a signal transduction cascade culminating in expression of defense responses that inhibit the pathogen and confer resistance. The hallmark of gene-for-gene resistance is a rapid programmed cell death of the cells in contact with the pathogen, called the hypersensitive response, or HR.
In many cases, gene-for-gene resistance reactions trigger another form of strong disease resistance called systemic acquired resistance, or SAR. Infection by a necrotizing pathogen (a pathogen that causes host cell death) causes a signal to be transmitted throughout the plant. In response, defense genes are activated in uninfected tissue, and the plant shows resistance to subsequent infection by a wide range of normally compatible pathogens. It is clear that salicylic acid (SA) plays a key role in establishment of SAR; resistant tissue contains elevated levels of SA, treatment of plants with SA induces defense gene expression and resistance, and SA is required in the responding tissue for defense gene expression and resistance. The question of whether or not SA is also the systemic signal has not yet been settled.
Genetic analyses using Arabidopsis-pathogen systems are being used to dissect the signaling pathways governing gene-for-gene resistance and SAR. Common pathogens used include the virulent
Pseudomonas syringae
strains
Pseudomonas syringae
pv.
maculicola
(Psm ES4326) and
Pseudomonas syringae
pv.
tomato
(Pst DC3000), Gram-negative bacteria that cause “bacterial speck” diseases in many crop plants, as well as isogenic strains carrying any of several cloned avirulence genes that elicit gene-for-gene resistance responses. In addition, a large number of isolates of
Peronospora parasitica
have been characterized and used to define many R genes in various Arabidopsis accessions. Several R genes have been isolated from Arabidopsis and other species. Comparison of the amino acid sequences of the R proteins has resulted in their division into several major classes.
Less progress has been made in identifying factors acting immediately downstream of R genes in gene-for-gene resistance. The Arabidopsis mutants ndr1 and eds1 have properties suggesting that NDR1 and EDS1 may be such factors. Mutations in either ndr1 or eds1 interfere with gene-for-gene resistance conferred by subsets of R genes.
Infection of Arabidopsis by
P. syringae
induces many defense responses, including synthesis of the phytoalexin camalexin, and expression of the pathogenesis-related genes PR-1 and PR-5, &bgr;-glucanase (BGL2), and anthranilate synthase (ASA1). Phytoalexins are small molecule broad-spectrum antimicrobial compounds synthesized by plants in response to pathogen attack. Camalexin is the only phytoalexin produced in significant quantities by Arabidopsis. Infection by a
P. syringae
strain carrying an avirulence gene such as avrRpt2 or treatment with SA induces SAR. SAR correlates with systemic expression of PR-1, PR-5, and BGL2.
SA-dependent signaling has been studied using genetic analysis in Arabidopsis. The central role of SA in defense response signaling was revealed by characterization of transgenic plants expressing nahG. The nahG transgene encodes salicylate hydroxylase, an enzyme that converts SA to catechol. Thus, nahG plants are unable to accumulate SA, and are conceptually similar to mutants deficient in SA. Arabidopsis nahG plants fail to develop SAR in response to SA or necrotizing pathogens. They are also compromised in local resistance, displaying reduced PR-1 expression in response to infection, susceptibility to pathogens that are normally avirulent as a consequence of gene-for-gene resistance, and heightened susceptibility to normally virulent pathogens. Although camalexin synthesis is not inducible by SA, nahG plants fail to synthesize camalexin in response to local Psm ES4326 infection, suggesting that SA is necessary, but not sufficient, for activation of camalexin synthesis. Taken together, these results show that SA is important in gene-for-gene resistance and in limiting growth of virulent pathogens, as well as in SAR.
Several Arabidopsis mutants that constitutively express SAR have been isolated. Many of these mutants are “lesion-mimics”, that is, they spontaneously develop necrotic lesions in the absence of any pathogen. After developing lesions, these plants accumulate high levels of SA, express PR-1 and are more resistant to pathogens. It is thought that lesion formation mimics the HR, thereby activating the SAR pathway in the rest of the plant. The lesion-mimic mutations appear to be acting upstream from SA in that they exhibit elevated SA levels and introduction of nahG reduces SA levels and abolishes PR-1 expression and resistance. In some, but not all lesion-mimics, introduction of nahG also abolishes lesion formation, strongly suggesting the existence of a positive feedback loop between cell death and SA accumulation. The cpr1 and cpr6 mutants constitutively express PR-1 and exhibit elevated SA levels, but do not spontaneously develop lesions. These mutations may define genes acting between lesion formation and SA accumulation. Importantly, lesion mimic mutants generally have greatly reduced vigor, and cpr1, cpr5, and cpr6 plants are dwarf, indicating that constitutive expression of defense responses may not be the best strategy for improving disease resistance in crops.
An Arabidopsis gene that has been variously named NPR1, NIM1, and SAI1, is required for SA-mediated disease resistance. SA treatment of npr1
im1 /sai1 mutants does not activate expression of PR-1, PR-5, or BGL2. When infected with a pathogen that induces SAR in wild-type plants, npr1
im1/sai1 mutants accumulate high levels of SA, but do not develop SAR, indicating that NPR1/NIM1/SAI1 acts downstream from SA. However, NPR1/NIM1/SAI1 is not required for camalexin synthesis, so the effect of SA on camalexin synthesis must be mediated by some other, as yet unknown, factor. Plants with npr1
im1/sai1 mutations display enhanced susceptibility to virulent pathogens, demonstrating that signal transduction downstream from NPR1/NIM1/SAI1 is important for restricting virulent pathogens as well as for SAR. NPR1/NIM1/SAI1 was recently cloned and shown to encode a protein containing ankyrin repeats.
Improving plant germplasm for increased resistance to disease is an agronomic goal of a high priority. Plants better able to respond to disease challenge in general, and via timely SA-induced

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