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pubmed-article:11115891pubmed:abstractTextWe have characterized developmental, environmental, and genetic regulation of abscisic acid-insensitive (ABI)4 gene expression in Arabidopsis. Although expressed most strongly in seeds, ABI4 transcripts are also present at low levels in vegetative tissue; vegetative expression is not induced by abscisic acid (ABA) or stress treatments. Comparison of transcript levels in mature seeds of ABA-insensitive, ABA-hypersensitive, ABA-deficient, or heterochronic mutants indicates that ABI4 expression is altered in only two of the backgrounds, the ABA-insensitive mutants abi1-1 and abi3-1. To determine whether ABI4 is necessary and/or sufficient for ABA response, we assayed the effects of loss of ABI4 function and ectopic ABI4 expression on growth and gene expression. We examined genetic interactions among three ABA response loci, ABI3, ABI4, and ABI5, by comparing phenotypes of mutants, ectopic expression lines, mutants carrying an ectopically expressed transgene, and the corresponding wild-type lines. Our results indicate some cross-regulation of expression among ABI3, ABI4, and ABI5 and suggest that they function in a combinatorial network, rather than a regulatory hierarchy, controlling seed development and ABA response.lld:pubmed
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pubmed-article:11115891pubmed:authorpubmed-author:LynchT JTJlld:pubmed
pubmed-article:11115891pubmed:authorpubmed-author:FinkelsteinR...lld:pubmed
pubmed-article:11115891pubmed:authorpubmed-author:SödermanE MEMlld:pubmed
pubmed-article:11115891pubmed:authorpubmed-author:BrocardI MIMlld:pubmed
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pubmed-article:11115891pubmed:dateRevised2010-9-14lld:pubmed
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pubmed-article:11115891pubmed:articleTitleRegulation and function of the Arabidopsis ABA-insensitive4 gene in seed and abscisic acid response signaling networks.lld:pubmed
pubmed-article:11115891pubmed:affiliationDepartment of Molecular, Cellular, and Developmental Biology, University of California, Santa Barbara, California 93106, USA.lld:pubmed
pubmed-article:11115891pubmed:publicationTypeJournal Articlelld:pubmed
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