Arabidopsis lenc1 mutant displays reduced ABA accumulation by low AtNCED3 expression under osmotic stress

The plant hormone, abscisic acid (ABA), is a main signal transducer that confers abiotic stress tolerance to plants. Although the pathway of ABA production and the genes catalyzing its biosynthesis are largely defined, the regulatory mechanism of ABA biosynthesis in response to abiotic stress remain...

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Published inJournal of plant physiology Vol. 168; no. 2; pp. 140 - 147
Main Authors Woo, Dong-Hyuk, Park, Hee-Yeon, Kang, In Soon, Lee, Sun-Young, Moon, Byoung Yong, Lee, Chin Bum, Moon, Yong-Hwan
Format Journal Article
LanguageEnglish
Published Munich Elsevier GmbH 15.01.2011
Elsevier
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Summary:The plant hormone, abscisic acid (ABA), is a main signal transducer that confers abiotic stress tolerance to plants. Although the pathway of ABA production and the genes catalyzing its biosynthesis are largely defined, the regulatory mechanism of ABA biosynthesis in response to abiotic stress remains much unknown. In this study, to identify upstream genes regulating ABA biosynthesis involved in abiotic stress signal transduction, Arabidopsis thaliana mutants with altered promoter activity of 9- cis- epoxycarotenoid dioxygenase 3 ( NCED3), a key gene in ABA biosynthesis, were identified and characterized. Among selected mutants, lenc1 (for low expression of NCED3 1 ) after dehydration treatment had lower AtNCED3 promoter activity compared with wild type. lenc1 mutation is recessive and is located on chromosome 4. Expression analysis of AtNCED3 and quantification of ABA levels showed that both the AtNCED3 transcripts and the endogenous ABA in lenc1 were less abundant than in wild type under dehydration treatments. The lenc1 was hypersensitive to methyl viologen (MV), LiCl, NaCl and high light. The aerial part of lenc1 lost water faster than wild type possibly due to a larger stomata opening. Our results suggest LENC1 might act as a positive regulator in AtNCED3 gene expression under osmotic stress.
Bibliography:http://dx.doi.org/10.1016/j.jplph.2010.06.006
ObjectType-Article-1
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ISSN:0176-1617
1618-1328
DOI:10.1016/j.jplph.2010.06.006