75 Integrating Membrane Transport with Male Gametophyte ... - TAIR

267 Identification of new actors of the hypersensitive cell death in Arabidopsis using AtMYB30
as a starting point.
Xavier DANIEL, Dominique ROBY
LIPM CNRS/INRA Toulouse
In an incompatible interaction, the most spectacular plant response is the Hypersensitive Response (HR), characterized
by the plant cell death at the site of the attempted infection by the pathogen. Few data are available on the regulators of this
cell death genetic program, tightly linked to plant resistance to pathogens. To identify such regulators, two approaches have
been developed in the lab: isolation of genes specifically induced during the HR (differential screenings), and isolation of
genes which mutation leads to an altered HR (screens for mutants displaying a lesion mimic phenotype or enhanced disease/
susceptibility phenotype). AtMYB30 was identified by differentially screening a cDNA library generated from Arabidopsis cell
suspensions grown in the presence of cycloheximide and inoculated by Xanthomonas campestris pv. campestris. AtMYB30
protein contains a domain displaying strong homologies to other plant and animal MYB proteins. Analysis of AtMYB30
expression during diverse interactions shows that maximal transcription clearly precedes the HR (1). AtMYB30 expression
is deregulated in Arabidopsis mutants affected in the control of the hypersensitive cell death, suggesting a strong correlation
between its expression and the initiation of the hypersensitive cell death. To get further insight into the role of AtMYB30
in this program, Arabidopsis and tobacco transgenic lines over-expressing AtMYB30 in sense (AtMYB30ox) and antisense
orientations were generated. Their response to avirulent and virulent bacterial and fungal pathogens display a modification
of the kinetics and intensity of the HR, as well as of disease resistance. These data demonstrate the positive regulator role
of AtMYB30 in the initiation of the hypersensitive cell death in response to pathogen attack (2). However, the absence of
spontaneous lesions in the AtMYB30ox plants, the altered resistance phenotype to avirulent pathogens, and the profound
modification of their susceptibility to virulent pathogens (HR-like phenotype) show that AtMYB30 cannot act by itself.
AtMYB30, being a positive regulator of the hypersensitive cell death and resistance in Arabidopsis in tobacco, and needing
other factor(s) to control the genetic program associated with the HR, is being used as a starting point for the identification
of new actors of this program. The methods used for this purpose, and the first identified candidates are presented.
1 Xavier Daniel et al., (1999).The Plant Journal, 20(1):57-66.
2 Fabienne Vailleau, Xavier Daniel et al.,(2002). PNAS, 99(15):10179-10184.
268 Relating Pathogen Infection and Host Genotype in Midwestern Arabidopsis Populations
Megan Dunning, Joy Bergelson
University of Chicago
The interaction between plants and pathogens is believed to be an important force shaping the ecology and evolution
of plant populations. For this to be true in a natural plant-pathogen system, host resistance and pathogen virulence must
vary according to host genotype. To test this prediction, leaf samples have been collected from Arabidopsis thaliana
populations in Indiana and Michigan. The growth of three known bacterial pathogens found in these fields (Pseudomonas
viridiflava, P. syringae and Xanthomonas campestris) was recorded in the collected leaves in order to assess pathogen load.
In the host, a set of SNP markers distributed across the genome has been selected to assess the genome-wide haplotype
for each A. thaliana plant sampled. By comparing naturally occurring pathogen load with host genotype, we can ask
whether pathogen growth is correlated with host frequency and relative growth of other pathogens.
After assessing the growth of these three pathogens in A. thaliana leaves, both individuals and local populations show
differences in infection prevalence and severity. Although these Arabidopsis populations have been previously shown to
have low genetic diversity compared to a worldwide sample, our preliminary genotyping suggests that previous studies
may have underestimated the genetic diversity in Midwestern populations. Nonetheless, several haplotypes are shared
among populations, allowing us to compare pathogen load across genetically identical individuals. By examining the
frequency and abundance of these pathogens in Midwestern populations of A. thaliana, we hope to clarify the importance
of host genotype for disease resistance in the field.