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The non‐ DNA ‐binding b HLH transcription factor PRE3/bHLH135/ATBS1/TMO7 is involved in the regulation of light signaling pathway in Arabidopsis
Author(s) -
Castelain Mathieu,
Le Hir Rozenn,
Bellini Catherine
Publication year - 2012
Publication title -
physiologia plantarum
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.351
H-Index - 146
eISSN - 1399-3054
pISSN - 0031-9317
DOI - 10.1111/j.1399-3054.2012.01600.x
Subject(s) - brassinosteroid , arabidopsis , biology , transcription factor , gene , meristem , microbiology and biotechnology , signal transduction , regulation of gene expression , genetics , dna , mutant
Plant basic Helix‐loop‐helix (bHLH) proteins are transcription factors that are involved in many developmental mechanisms, including light signaling and hormone homeostasis. Some of them are non‐DNA‐binding proteins and could act as dominant negative regulators of other bHLH proteins by forming heterodimers, in a similar way to animal inhibitor of DNA‐binding proteins. It has been recently reported that several non‐DNA‐binding bHLHs are involved in light signaling ( KDR/PRE6 ), gibberellic acid signaling ( PRE1/BNQ1/bHLH136 ) or brassinosteroid signaling ( ATBS1 ). Here we report that Arabidopsis lines overexpressing the PRE3/bHLH135/ATBS1/TMO7 gene are less responsive to red, far‐red and blue light than wild‐type which is likely to explain the light hyposensitive phenotype displayed when grown under white light conditions. Using quantitative polymerase chain reaction, we show that the expression of PRE3 and KDR/PRE6 genes is regulated by light and that light‐related genes are deregulated in the PRE3‐ox lines. We show that PRE3 is expressed in the shoot and root meristems and that PRE3‐ox lines also have a defect in lateral root development. Our results not only suggest that PRE3 is involved in the regulation of light signaling, but also support the hypothesis that non‐DNA‐binding bHLH genes are promiscuous genes regulating a wide range of both overlapping and specific regulatory pathways.