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Structural analogs of ABA reveal novel features of ABA perception and signaling in Arabidopsis
Author(s) -
Huang Daiqing,
Jaradat Masrur R.,
Wu Weiren,
Ambrose Stephen J.,
Ross Andrew R.,
Abrams Suzanne R.,
Cutler Adrian J.
Publication year - 2007
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.2007.03056.x
Subject(s) - abscisic acid , arabidopsis , gene , mutant , arabidopsis thaliana , gene expression , biology , plant hormone , microbiology and biotechnology , biochemistry , chemistry
Summary Changes in gene expression produced by the application of (+)‐abscisic acid (ABA) to Arabidopsis thaliana plants were compared with changes produced by the ABA structural analogs (−)‐ABA, (+)‐8′‐acetylene ABA and (−)‐2′,3′‐dihydroacetylenic abscisyl alcohol. The maximum expression of many rapidly (+)‐ABA‐induced genes occurred prior to peak hormone accumulation, suggesting negative feedback regulation that may be mediated by the induction of genes encoding PP2C‐type protein phosphatases. For most rapidly (+)‐ABA‐induced genes, expression was delayed in ABA analog treatments although analogs accumulated to higher levels than did (+)‐ABA. For each analog, some genes exhibited a hypersensitive response to the analog and some genes were less sensitive to the analog than to (+)‐ABA. Variations in the sensitivity of gene expression to (+)‐ABA and analogs reflect the different structural requirements of two or more classes of hormone receptors. By using ABA analogs to reveal and confirm weakly (+)‐ABA‐regulated genes, we estimate that 14% of Arabidopsis genes are ABA‐regulated in aerial tissues. Treatments with the analog (+)‐8′‐acetylene ABA (PBI425) led to the identification of new ABA‐regulated genes. As an example, the transcription factor MYBR1 was significantly induced by PBI425, but not by (+)‐ABA, and is shown to play a role in ABA signaling by phenotypic analysis of gain‐of‐function and loss‐of‐function mutants.