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The Arabidopsis her1 mutant implicates GABA in E ‐2‐hexenal responsiveness
Author(s) -
Mirabella Rossana,
Rauwerda Han,
Struys Eduard A.,
Jakobs Cornelis,
Triantaphylidès Christian,
Haring Michel A.,
Schuurink Robert C.
Publication year - 2008
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2007.03323.x
Subject(s) - jasmonic acid , arabidopsis , arabidopsis thaliana , mutant , salicylic acid , gaba transaminase , biology , biochemistry , gene , microbiology and biotechnology , chemistry , enzyme , glutamate decarboxylase
Summary When wounded or attacked by herbivores or pathogens, plants produce a blend of six‐carbon alcohols, aldehydes and esters, known as C6‐volatiles. Undamaged plants, when exposed to C6‐volatiles, respond by inducing defense‐related genes and secondary metabolites, suggesting that C6‐volatiles can act as signaling molecules regulating plant defense responses. However, to date, the molecular mechanisms by which plants perceive and respond to these volatiles are unknown. To elucidate such mechanisms, we decided to isolate Arabidopsis thaliana mutants in which responses to C6‐volatiles were altered. We observed that treatment of Arabidopsis seedlings with the C6‐volatile E ‐2‐hexenal inhibits root elongation. Among C6‐volatiles this response is specific to E ‐2‐hexenal, and is not dependent on ethylene, jasmonic and salicylic acid. Using this bioassay, we isolated 18 E ‐2‐hexenal‐response ( her ) mutants that showed sustained root growth after E ‐2‐hexenal treatment. Here, we focused on the molecular characterization of one of these mutants, her1 . Microarray and map‐based cloning revealed that her1 encodes a γ‐amino butyric acid transaminase (GABA‐TP), an enzyme that degrades GABA. As a consequence of the mutation, her1 plants accumulate high GABA levels in all their organs. Based on the observation that E ‐2‐hexenal treatment induces GABA accumulation, and that high GABA levels confer resistance to E ‐2‐hexenal, we propose a role for GABA in mediating E ‐2‐hexenal responses.