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Herbivory‐induced jasmonates constrain plant sugar accumulation and growth by antagonizing gibberellin signaling and not by promoting secondary metabolite production
Author(s) -
Machado Ricardo A. R.,
Baldwin Ian T.,
Erb Matthias
Publication year - 2017
Publication title -
new phytologist
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.742
H-Index - 244
eISSN - 1469-8137
pISSN - 0028-646X
DOI - 10.1111/nph.14597
Subject(s) - jasmonate , gibberellin , biology , metabolite , sugar , herbivore , secondary metabolite , plant defense against herbivory , botany , methyl jasmonate , manduca sexta , biochemistry , arabidopsis , gene , insect , mutant
Summary Plants respond to herbivory by reconfiguring hormonal networks, increasing secondary metabolite production and decreasing growth. Furthermore, some plants display a decrease in leaf energy reserves in the form of soluble sugars and starch, leading to the hypothesis that herbivory‐induced secondary metabolite production and growth reduction may be linked through a carbohydrate‐based resource trade‐off. In order to test the above hypothesis, we measured leaf carbohydrates and plant growth in seven genetically engineered Nicotiana attenuata genotypes that are deficient in one or several major herbivore‐induced, jasmonate‐dependent defensive secondary metabolites and proteins. Furthermore, we manipulated gibberellin and jasmonate signaling, and quantified the impact of these phytohormones on secondary metabolite production, sugar accumulation and growth. Simulated herbivore attack by Manduca sexta specifically reduced leaf sugar concentrations and growth in a jasmonate‐dependent manner. These effects were similar or even stronger in defenseless genotypes with intact jasmonate signaling. Gibberellin complementation rescued carbohydrate accumulation and growth in induced plants without impairing the induction of defensive secondary metabolites. These results are consistent with a hormonal antagonism model rather than a resource–cost model to explain the negative relationship between herbivory‐induced defenses, leaf energy reserves and growth.