FIERY1 regulates light-mediated repression of cell elongation and flowering time via its 3'(2'),5'-bisphosphate nucleotidase activity

Light is one of the most important environmental factors that regulate plant development. Here we report that a mutation in the Arabidopsis FIERY1 gene (FRY1) caused a shortened hypocotyl and shorter petioles, most dramatically under low-intensity red light and less pronounced under far-red and blue...

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Published inThe Plant journal : for cell and molecular biology Vol. 58; no. 2; pp. 208 - 219
Main Authors Kim, Byung-Hoon, von Arnim, Albrecht G
Format Journal Article
LanguageEnglish
Published Oxford, UK Oxford, UK : Blackwell Publishing Ltd 01.04.2009
Blackwell Publishing Ltd
Blackwell
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Summary:Light is one of the most important environmental factors that regulate plant development. Here we report that a mutation in the Arabidopsis FIERY1 gene (FRY1) caused a shortened hypocotyl and shorter petioles, most dramatically under low-intensity red light and less pronounced under far-red and blue-light conditions. Furthermore, the fry1 mutant flowered late, probably due to a reduced level of FLOWERING LOCUS T (FT) transcript. However, although the transcript level of FRY1 was light-regulated, the chlorophyll level and the expression of typical light-regulated genes were not affected in the fry1 mutant. FRY1 is known as a regulator of abiotic stress responses, and its protein product has dual enzymatic activity comprising inositol polyphosphate-1-phosphatase and 3'(2'),5'-bisphosphate nucleotidase activity. Genetic complementation data obtained using cDNA of the FRY1 paralog AHL (Arabidopsis HAL2-like) and the similar phenotype of an xrn2/xrn3 double mutant suggest that FRY1 attenuates light responses via its 3'(2'),5'-bisphosphate nucleotidase activity rather than its inositol polyphosphate-1-phosphatase activity. We discuss the relationship between the FRY1-associated nucleotidase activity, a step in the pathway for sulfur metabolism and utilization, and the Arabidopsis light response.
Bibliography:http://dx.doi.org/10.1111/j.1365-313X.2008.03770.x
ISSN:0960-7412
1365-313X
DOI:10.1111/j.1365-313X.2008.03770.x