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Investigating the role of putative defense metabolites in Picea abies by genetic transformation

Applicant Dr. Axel Schmidt, since 2/2008
Subject Area Forestry
Term from 2005 to 2009
Project identifier Deutsche Forschungsgemeinschaft (DFG) - Project number 20783791
 
Final Report Year 2009

Final Report Abstract

Norway spruce, Picea abies, is an important forest tree for the production of wood and fibre. Under conditions when spruce trees are under abiotic stress, trees are attacked by the European bark beetle, Ips typographus, and its fungal associate Ceratocystis polonica. This beetle-fungus association can cause large losses in natural forests and commercial plantations. The goal of this project was to study defence responses of spruce to simulations of bark beetle attack, such as wounding and artificial fungus inoculation. Initial studies on transcriptional responses of genetically non-uniform spruce saplings to C. polonica infection showed that phenotypic variation in saplings was too high for making statistically supported inferences about the defence response. Further studies on clonal saplings showed a possible involvement of the phenylpropanoid biosynthesis pathway in spruce defence to fungal attack. Spruce saplings significantly increased transcription of enzymes involved in stilbene and flavonoid biosynthesis upon C. polonica attack. Transcript accumulation was mirrored in stilbene and flavonoid metabolite accumulation with the exception of stilbene accumulation 14-28 days after the onset of infection. Decreases in stilbene content in infected saplings were due to fungal conversion of stilbenes into dimers and breakdown products. By using fungi with differing virulence for inoculation trials, it was also possible to show that early recognition of the pathogen enabled saplings to initiate earlier responses which led to shorter fungal lesions of infected sapling stems. Further investigations into the ecological significance of flavonoids and stilbenes have been initiated by using transgenic spruce lines overexpressing selected proteins putatively involved in phenylpropanoid biosynthesis.

 
 

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