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15th International Conference on Arabidopsis Research - TAIR

15th International Conference on Arabidopsis Research - TAIR

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T05-021<br />

Mutati<strong>on</strong>s in <strong>Arabidopsis</strong> RIN4 that affect the<br />

virulence of AvrRpm1, AvrB, and AvrRpt2 and R-gene<br />

mediated HR.<br />

Han Suk Kim(1), Darrell Desveaux(1), Alex Singer(2), John S<strong>on</strong>dek(2), Jeff Dangl(1)<br />

1-Department of Biology, University of North Carolina, Chapel Hill<br />

2-Department of Pharmacology, University of North Carolina, Chapel Hill<br />

RPM1-interacting protein 4 or RIN4 of <strong>Arabidopsis</strong> thaliana, is targeted<br />

by three different Pseudom<strong>on</strong>as syringae Type III effector proteins, AvrB,<br />

AvrRpm1, and AvrRpt2. Up<strong>on</strong> infecti<strong>on</strong> with P. syringae carrying either avrB<br />

or avrRpm1of susceptible hosts (rpm1), RIN4 becomes phosphorylated and<br />

plant disease occurs. During infecti<strong>on</strong> of susceptible hosts lacking RPS2<br />

with P. syringae carrying avrRpt2, RIN4, however, is thought to be degraded-<br />

proteolytically, perhaps c<strong>on</strong>tributing to pathogen growth. In RPS2 plants, the<br />

AvrRpt2-driven disappearance of RIN4 is required to activate RPS2 functi<strong>on</strong>.<br />

To determine whether or not RIN4 phosphorylati<strong>on</strong> or proteolytic cleavage of<br />

RIN4 is required for the virulence functi<strong>on</strong> of AvrB and AvrRpm1, or AvrRpt2,<br />

we have made mutati<strong>on</strong>s in putative phosphorylati<strong>on</strong> sites in RIN4 as well<br />

as two highly c<strong>on</strong>served cysteine protease cleavage sites at the N- and<br />

C-terminal ends of RIN4. We present data <strong>on</strong> transgenic <strong>Arabidopsis</strong> plants<br />

transformed with either the RIN4 phosphorylati<strong>on</strong> mutants or the N- and<br />

C-terminal cysteine protease cleavage site mutants. We show the effect of<br />

the RIN4 mutati<strong>on</strong>s <strong>on</strong> the ability of AvrB or AvrRpm1 and AvrRpt2 to cause<br />

disease <strong>on</strong> susceptible hosts. In additi<strong>on</strong>, the regi<strong>on</strong> of RIN4 resp<strong>on</strong>sible for<br />

the interacti<strong>on</strong> with AvrB c<strong>on</strong>tains <strong>on</strong>e of the c<strong>on</strong>served cysteine protease<br />

cleavage sites. We therefore also show what affect the RIN4 mutati<strong>on</strong>s has<br />

<strong>on</strong> the ability of AvrRpt2 to interfere with the avirulence functi<strong>on</strong> of AvrB or<br />

AvrRpm1. Since modificati<strong>on</strong>s of RIN4 are detected by RPM1 and RPS2, we<br />

also show the effect of the RIN4 mutati<strong>on</strong>s <strong>on</strong> R-gene mediated hypersensitive<br />

resp<strong>on</strong>se (HR).<br />

15 th <str<strong>on</strong>g>Internati<strong>on</strong>al</str<strong>on</strong>g> <str<strong>on</strong>g>C<strong>on</strong>ference</str<strong>on</strong>g> <strong>on</strong> <strong>Arabidopsis</strong> <strong>Research</strong> 2004 · Berlin<br />

T05-022<br />

Searching For Novel Comp<strong>on</strong>ents Involved In Plant<br />

N<strong>on</strong>host Disease Resistance In <strong>Arabidopsis</strong><br />

Landtag, Jörn(1), Westphal, Lore(1), Lipka, Volker(1), Dittgen, Jan(1), Schulze-<br />

Lefert, Paul(1), Scheel, Dierk(1), Rosahl, Sabine(1, 4)<br />

1-Leibniz Institute of Plant Biochemistry<br />

2-Leibniz Institute of Plant Biochemistry<br />

3-Max-Planck-Institut für Züchtungsforschung Köln<br />

4-Max-Planck-Institut für Züchtungsforschung Köln<br />

5-Max-Planck-Institut für Züchtungsforschung Köln<br />

6-Leibniz Institute of Plant Biochemistry<br />

7-Leibniz Institute of Plant Biochemistry<br />

N<strong>on</strong>host disease resistance is the major form of disease resistance by plants<br />

which is effective against the majority of parasitic microorganisms such as<br />

bacteria, fungi and oomycetes. Plants have evolved several defence mechanisms<br />

to protect themselves against invading pathogens. These include<br />

preformed physical barriers like plant cytoskelet<strong>on</strong> as well as inducible<br />

mechanisms like the hypersensitive resp<strong>on</strong>se with cell death.<br />

Here, we describe the characterizati<strong>on</strong> of a n<strong>on</strong>host-pathosystem involving<br />

the model plant <strong>Arabidopsis</strong> and the ec<strong>on</strong>omically important oomycete<br />

pathogen Phytophthora infestans. Cytological analysis of <strong>Arabidopsis</strong> wildtype<br />

plants challenged with Phytophthora infestans spores revealed that the cell<br />

wall penetrati<strong>on</strong> attempts are usually aborted and <strong>on</strong>ly few spores can trigger<br />

a hypersensitive resp<strong>on</strong>se with cell death.<br />

To find novel comp<strong>on</strong>ents of the n<strong>on</strong>host disease resistance we started<br />

an EMS-mutagenesis approach. A microscope-based screen for altered<br />

resistance phenotypes up<strong>on</strong> P. infestans challenge c<strong>on</strong>ducted with more<br />

than 70.000 M2 plants allowed the isolati<strong>on</strong> of several mutant plants with an<br />

enhanced penetrati<strong>on</strong> frequency phenotype.<br />

T05 Interacti<strong>on</strong> with the Envir<strong>on</strong>ment 2 (Biotic)

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