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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 47 X X I V S P P S C O N G R E S S 2 0 1 1 Session 10/14. Bioenergy and primary and secondary metabolism WHAT IS THE TRANSPORT MECHANISM OF MONOLIGNOLS IN LIGNIFYING XYLEM OF NORWAY SPRUCE? Kurt V. Fagerstedt 1 , Junko Takahashi 2 , Enni Väisänen 1,3 , Anna Kärkönen 3,4 1 Department of Biosciences, Division of Plant Biology, University of Helsinki, Finland 2 Umeå Plant Science Center, Umeå University, Umeå, Sweden 3 Department of Agricultural Sciences, University of Helsinki, Helsinki, Finland 4 MTT Agrifood Research, University of Helsinki,Helsinki, Finland E-mail: kurt.fagerstedt@helsinki.fi While the biosynthesis of monolignols is relatively well characterized, the transport of monolignols into the apoplastic space in developing xylem is known to a far lesser extent. Our aim is to understand the cell and molecular biology of the transport mechanisms. We can envisage three possibilities for the transport: Golgi vesicle-mediated transport, plasma membrane-located ABC-type transporter proteins or membrane channel proteins, and diffusion based on the hydrophobic properties of the monolignols. While the Golgi vesicle-based transport has been shown plausibly not to be the transport mechanism [1], we are testing the other possibilities by using 14 C-labelled phenylalanine and monolignols containing a radioactive or fluorescent label together with transporter inhibitors in a Norway spruce (Picea abies) tissue culture system that produces extracellular lignin [2]. Also plasma membranes isolated from lignifying xylem of mature trees are used in the experiments. As a background for the present study, we have done an extensive database search on genes related to transport phenomena and their expression levels in different tissues of conifers. The latest results of the ongoing work will be discussed. References [1] Kaneda et al., Plant Physiol. 2008 [2] Kärkönen et al., Physiol. Plant. 2002
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 Session 10/14. Bioenergy and primary and secondary metabolism CAROTENOID BIOSYNTHESIS, STABILIZATION AND DEGRADATION, WHICH DETERMINE COLOR INTENSITY IN PETALS OFYELLOW-PIGMENTED CUT ROSES, ARE REGULATED BY APPLICATION OF METHYL JASMONATE Alon Glick 1 , Sonia Philosoph-Hadas 1 , Alexander Vainstein 2 ,Shimon Meir 1 1 Department of Postharvest Science of Fresh Produce, ARO, TheVolcani Center, Bet-Dagan, Israel 2 The Robert H. Smith Institute of Plant Sciences and Genetics in Agriculture, The Hebrew University of Jerusalem, Jerusalem, Israel 3 Department of Genetics, The Hebrew University of Jerusalem, Jerusalem, Israel 4 Department of Plant Pathology and Weed Research, TheVolcani Center, Bet-Dagan, Israel E-mail: shimonm@volcani.agri.gov.il Various yellow-pigmented cut rose (Rosa hybrida) cultivars such as 'Frisco' show color fading. The color intensity and the petal carotenoid content increased during the first two days of vase life, and gradually decreased thereafter. Application of methyl jasmonate (MJ) to the cut roses retained their petal color intensity and carotenoid content throughout vase life. Our analysis show that the decrease in carotenoid content resulted from both decreased carotenoid biosynthesis and increased carotenoid degradation, mainly of the yellow pigments violaxanthin, antheraxanthin and neoxanthin. The reduction in carotenoid biosynthesis resulted from decreased expression of two genes encoding two key enzymes in the pathway,phytoene synthase (Psy) and Ζcarotenedesaturase (Zds). The increase in carotenoid degradation resulted from increased expression of the plastidic carotenoid cleavage dioxygenase (CCD4) gene, which coincided with decreased content of the plastoglobulin chromoplast protein C (CHRC) and plastoglobule decomposition. MJ treatment inhibited petal color fading by increasing carotenoid biosynthesis and inhibiting carotenoid degradation. Taken together, our results suggest that MJ treatment regulates the three different processes that determine color intensity in yellow-pigmented rose petals, namely: carotenoid biosynthesis by increasingPsy and Zds expression; stabilizing the plastoglobules by increasing CHRC content, and carotenoid degradation by inhibiting CCD4 expression. 48 X X I V S P P S C O N G R E S S 2 0 1 1
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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 47: A B S T R A C T B O O K - A B S T R
Page 51 and 52: Session 13.Pathogen defense and pla
Page 53 and 54: 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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