15th International Conference on Arabidopsis Research - TAIR

T05-073
The PEN1 syntaxin defines a novel compartment
upon fungal attack and is required for the timely
assembly of papilla
Farhah Assaad(1, 3), Jin-Long Qiu(2), Heather Youngs(3), David Ehrhardt(3),
Laurent Zimmerli(3), Monika Kalde(4), Gehard Wanner(5), Scott Peck(4), Katrina
Ramonell(3), Herb Edwards(6), Chris Somerville(3), Hans Thordal-Christensen(2)
1-Botany, TU Munich
2-Plant Research Laboratory, Risoe
3-Carnegie Institution, Plant Biology
4-Sainsbury Laboratory
5-Botany, LMU Munich
6-Western Illinois Univeristy
Attack by the host powdery mildew Erysiphe cichoracearum usually results in
successful penetration and rapid proliferation of the fungus on Arabidopsis.
By contrast, the non-host barley powdery mildew Blumeria graminis f. sp.
hordei (Bgh) typically fails to penetrate Arabidopsis epidermal cells. In both
instances the plant secretes cell wall appositions or papillae beneath the
penetration peg of the fungus. Genetic screens for mutations that result in increased
penetration of Bgh on Arabidopsis have recently identified the PEN1
syntaxin (Collins et al., 2003). Here we examine the role of PEN1’s closest
homologue, SYP122, identified as a syntaxin whose expression is responsive
to disease. pen1 syp122 double mutants are both dwarfed and necrotic,
suggesting that the two syntaxins have overlapping functions. Although
syp122-1 and mur1 mutants have considerably more pronounced primary
cell wall defects than pen1 mutants, SYP122 and MUR1 have only a very
subtle, yet measurable, effect on penetration resistance. Upon fungal attack,
PEN1 appears to be actively recruited to papillae, and there is a 2-hour delay
in papillae formation in the pen1-1 mutant. We conclude that, while SYP122
may be involved in diffuse secretion, PEN1 is involved in the polarized secretion
events that give rise to papilla formation.
Collins, N.C., Thordal-Christensen, H., Lipka, et al., 2003. Nature 425, 973-7
15 th <strong>International</strong> <strong>Conference</strong> on Arabidopsis Research 2004 · Berlin
T05-074
Enhanced resistance to Cucumber mosaic virus in
the Arabidopsis thaliana ssi2 mutant is mediated via
an SA-independent mechanism
Ken-Taro Sekine(1), Ashis Nandi(2), Takeaki Ishihara(1), Shu Hase(1), Masato
Ikegami(1), Jyoti Shah(2), Hideki Takahashi(1)
1-Department of Life Science, Graduate School of Agricultural Science, Tohoku University, 1-1
Tsutsumidori-Amamiyamachi, Aoba-ku, Sendai 981-8555, Japan
2-Division of Biology and the Molecular, Cellular and Developmental Biology Program, Kansas
State University, 303 Ackert Hall, Manhattan 66506-4901, U.S.A
The Arabidopsis thaliana SSI2 gene encodes a plastid-localized stearoyl-ACP
desaturase. The recessive ssi2 mutant allele confers constitutive accumulation
of the pathogenesis-related-1 (PR-1) gene transcript and salicylic
acid (SA), and enhanced resistance to bacterial and oomycete pathogens.
In addition, the ssi2 mutant is a dwarf and spontaneously develops lesions
containing dead cells (Shah et al., 2001). Here, we show that the ssi2
mutant also confers enhanced resistance to Cucumber mosaic virus (CMV).
Compared with the wild type plant, viral multiplication and systemic spread
were diminished in the ssi2 mutant plant. However, unlike the ssi2-conferred
resistance to bacterial and oomycete pathogens, the ssi2-conferred enhanced
resistance to CMV was retained in the SA-deficient ssi2 nahG plant. In
addition, SA application was not effective in limiting CMV multiplication and
systemic spread in the CMV-susceptible wild type plant. The acd1, acd2 and
cpr5 mutants which, like the ssi2 mutant, accumulate elevated SA levels,
constitutively express the PR-1 gene, spontaneously develop lesions containing
dead cells and are dwarfs, are, however, fully susceptible to CMV. Our
results suggest that the basal resistance to CMV is enhanced specifically in
the ssi2 mutant plant and that dwarfing, cell death and constitutive activation
of SA signaling are not important for the ssi2-conferred enhanced resistance
to CMV. However, the sfd1 and sfd4 mutations which, in addition to disturbing
the ssi2-confers phenotypes containing dwarfing, spontaneously developing
lesions and constitutively accumulating elevated SA levels, also affect lipid
metabolism, suppress the ssi2-conferred enhanced resistance to CMV, thus
implicating a lipid or lipids in the ssi2-conferred resistance to CMV. Interestingly,
the ssi2-conferred resistance to CMV was compromised in the ssi2 eds5
plant, suggesting the involvement of a SA-independent, EDS5-dependent
mechanism in the ssi2-conferred resistance to CMV (Sekine et al., 2004).
Shah et al., Plant J., 25:563-574. (2001)
Sekine et al., Mol. Plant-Microbe Interact., 17:623-632. (2004)
T05 Interaction with the Environment 2 (Biotic)