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A B S T R A C T B O O K – A B S T R A C T S O F T A L K S 51 X X I V S P P S C O N G R E S S 2 0 1 1 Session 13.Pathogen defense and plant desease PSEUDOMONAS SYRINGAE PV.PHASEOLICOLA AND DICKEYA DADANTII 3937: TWO PATHOGENIC LIFE-STYLES ANALYSED BY IMAGING TECHNIQUES M. Luisa Pérez-Bueno 1 , Emilia López-Solanilla 2 , Mónica Pineda 1 , Elena Díaz Casado, Cayo Ramos 3 , Pablo Rodríguez-Palenzuela 2 , Matilde Barón 1 1 Estación Experimental del Zaidín, CSIC, Granada, Spain 2 Centro de Biotecnología y Genómica de Plantas, Universidad Politécnica de Madrid - Instituto Nacional de Investigación y Tecnología Agraria y Alimentaria, Madrid, Spain 3 Area of Genetics, University of Malaga, Malaga, Spain E-mail: marisa.perez@eez.csic.es P. syringaepv. phaseolicola (Pph) and D. dadantii (D.d.) 3937 are model organisms for two very different “pathogenic life-styles”. The first one is the causal agent of halo blight disease of beans, characterized by small watersoaked spots which gradually turn necrotic, and become surrounded by a wide chlorotic halo (caused by the effect of a nonhost specific toxin produced by the bacteria). The second one is the causal agent of bacterial soft rot in vegetables. This disease occurs most commonly on fleshy storage tissues. Both pathogens cause great losses in crop production worldwide. Chlorophyll fluorescence (Chl-F) and blue-green fluorescence (BGF) techniques are sensitive and specific tools which provide information about the primary and secondary metabolism in plants, respectively. Chl-F, BGF and temperature leaf patterns obtained by imaging techniques were shown to be in correspondence with pathogen distribution and symptom development during viral pathogenesis. In the present work, the systemic infection of D.d. 3937 in N. benthamiana and Pph in Phaseolus vulgaris have been studied by these imaging techniques to understand the impact of these pathogens in plant physiology. Acknowledgements Financial support: MCINN-FEDER/AGL2008-00214, CVI 03475 (Junta de Andalucía). MLPB was recipient of a CSIC-JAE Doc contract.
Session 13.Pathogen defense and plant desease A B S T R A C T B O O K – A B S T R A C T S O F T A L K S CELL DEATH AND RESISTANCE 2 GENE IS A NEGATIVE REGULATOR OF CELL DEATH AND ENCODES AN AAA-TYPE ATPASE Hann Ling Wong 1 , Masayuki Isshiki 2 , Tsutomu Kawasaki 3 , Ko Shimamoto 4 1 Department of Biological Science, Universiti Tunku Abdul Rahman, Kampar, Malaysia 2 Kihara Institute for Biological Research, Yokohama City University, Yokohama, Japan 3 Department of Bioscience, Kinki University, Nara, Japan 4 Laboratory of Plant Molecular Genetics, Nara Institute of Science and Technology, Ikoma, Japan E-mail: hlwong2007@gmail.com The cell death and resistance (cdr2) mutant rice plants display a spontaneous cell death phenotype that resembles disease symptoms even without pathogen infection. This mutant belongs to the initiation class of lesion mimic mutant. Previously, we found that cdr2 mutant plants exhibit enhanced resistance to rice blast fungus infection. Suspensioncultured cdr2 cells also showed elevated defense-related genes expression and higher calyculinA-induced H2O2 production. In this study, we have localized the cdr2 mutation by map-based cloning. We further sequenced the candidate ORFs around the localized region and revealed that the cdr2 mutation is probably caused by a single-base (G to A) substitution, resulting in a Gly to Arg change in an ORF encoding an AAA-type ATPase. We analyzed the expression pattern of the Cdr2 gene by RT-PCR and found that its expression is ubiquitous in all rice tissues examined. Overexpression of Cdr2 gene in the cdr2 mutant complemented the lesion mimic phenotype and suppressed the cdr2 mutation-induced elevation defense-related genes. Furthermore, co-expression of Cdr2 gene suppressed Bax-induced cell death in Nicotiana benthamiana. Taken together, Cdr2 may function as a negative regulator in regulating cell death and defense response. 52 X X I V S P P S C O N G R E S S 2 0 1 1
Page 1 and 2: ��
Page 3 and 4: Foreword eword ord A B S T R A C T
Page 5 and 6: Program of the Congress gram of the
Page 7 and 8: A B S T R A C T B O O K - P R O G R
Page 9 and 10: A B S T R A C T B O O K - P R O G R
Page 11 and 12: Plenary session 1 A B S T R A C T B
Page 13 and 14: Plenary session 2 THE BIOLOGY OF AL
Page 15 and 16: Session 1. Biotechnology and synthe
Page 17 and 18: Session 1. Biotechnology and synthe
Page 19 and 20: Session 2. Systems biology and -omi
Page 21 and 22: Session 2. Systems biology and -omi
Page 23 and 24: A B S T R A C T B O O K - A B S T R
Page 27 and 28: Pleanary session 4 A B S T R A C T
Page 29 and 30: Invited talk 4 A B S T R A C T B O
Page 31 and 32: Session 5.Cell biology A B S T R A
Page 33 and 34: Session 6.Organelle biology A B S T
Page 35 and 36: Session 6.Organelle biology A B S T
Page 37 and 38: Session 7.Development A B S T R A C
Page 39 and 40: Session 8.Signalling A B S T R A C
Page 41 and 42: Pleanary session 6 A B S T R A C T
Page 51: Session 13.Pathogen defense and pla
Page 67 and 68: Sapporo Medical University, Sapporo
Page 91 and 92: SCF = A B S T R A C T B O O K - A B
Page 93 and 94: A B S T R A C T B O O K - L I S T O
Page 95 and 96: A B S T R A C T B O O K - L I S T O
Page 97 and 98: Sponsors onsors ors A B S T R A C T

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