Send to

Choose Destination
See comment in PubMed Commons below
Plant Physiol. 2002 Aug;129(4):1533-43.

Regulation and role of the Arabidopsis abscisic acid-insensitive 5 gene in abscisic acid, sugar, and stress response.

Author information

Department of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California 93106, USA.


Abscisic acid (ABA) and stress response from late embryonic growth through early seedling development is regulated by a signaling network that includes the Arabidopsis ABA-insensitive (ABI)5 gene, which encodes a basic leucine zipper transcription factor. We have characterized genetic, developmental, and environmental regulation of ABI5 expression. Although expressed most strongly in seeds, the ABI5 promoter is also active in vegetative and floral tissue. Vegetative expression is strongly induced by ABA, and weakly by stress treatments during a limited developmental window up to approximately 2 d post-stratification, but ABA and some stresses can induce expression in specific tissues at later stages. ABI5 expression is autoregulated in transgenic plants and yeast (Saccharomyces cerevisiae), and stress response appears to involve ABI5-dependent and -independent mechanisms. To determine whether ABI5 is necessary and/or sufficient for ABA or stress response, we assayed the effects of increased ABI5 expression on growth and gene expression. Although overexpression of ABI5 confers hypersensitivity to ABA and sugar, as previously described for ABI4 and ABI3 overexpression lines, it has relatively limited effects on enhancing ABA-responsive gene expression. Comparison of expression of eight ABI5-homologous genes shows overlapping regulation by ABI3, ABI4, and ABI5, suggestive of a combinatorial network involving positive and negative regulatory interactions.

[Indexed for MEDLINE]
Free PMC Article
PubMed Commons home

PubMed Commons

How to join PubMed Commons

    Supplemental Content

    Full text links

    Icon for HighWire Icon for PubMed Central
    Loading ...
    Support Center