Effect of Drought and Methyl Jasmonate Treatment on Primary and Secondary Isoprenoid Metabolites Derived from the MEP Pathway in the White Spruce Picea glauca

GND
1251862411
ORCID
0000-0002-9381-5318
Affiliation
Max Planck Institute for Chemical Ecology, Jena
Perreca, Erica;
GND
1189105152
ORCID
0000-0003-4097-6975
Affiliation
Max Planck Institute for Chemical Ecology, Jena
Eberl, Franziska;
GND
1306228190
Affiliation
Max Planck Institute for Chemical Ecology, Jena
Santoro, Maricel Valeria;
Affiliation
Zeiselhof Research Farm, Pretoria 0102, South Africa;
Wright, Louwrance Peter;
GND
1306228875
ORCID
0000-0002-4318-0799
Affiliation
Max Planck Institute for Chemical Ecology, Jena
Schmidt, Axel;
GND
1128621657
Affiliation
Max Planck Institute for Chemical Ecology, Jena
Gershenzon, Jonathan

White spruce ( Picea glauca ) emits monoterpenes that function as defensive signals and weapons after herbivore attack. We assessed the effects of drought and methyl jasmonate (MeJA) treatment, used as a proxy for herbivory, on monoterpenes and other isoprenoids in P. glauca . The emission of monoterpenes was significantly increased after MeJA treatment compared to the control, but drought suppressed the MeJA-induced increase. The composition of the emitted blend was altered strongly by stress, with drought increasing the proportion of oxygenated compounds and MeJA increasing the proportion of induced compounds such as linalool and ( E )-β-ocimene. In contrast, no treatment had any significant effect on the levels of stored monoterpenes and diterpenes. Among other MEP pathway-derived isoprenoids, MeJA treatment decreased chlorophyll levels by 40%, but had no effect on carotenoids, while drought stress had no impact on either of these pigment classes. Of the three described spruce genes encoding 1-deoxy-D-xylulose-5-phosphate synthase (DXS) catalyzing the first step of the MEP pathway, the expression of only one, DXS2B , was affected by our treatments, being increased by MeJA and decreased by drought. These findings show the sensitivity of monoterpene emission to biotic and abiotic stress regimes, and the mediation of the response by DXS genes.

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