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Plant and Cell Physiology, 2003, Vol. 44, No. 8 868-874
© 2003 Oxford University Press


Short Communications

The Type-A Response Regulator, ARR15, Acts as a Negative Regulator in the Cytokinin-Mediated Signal Transduction in Arabidopsis thaliana

Takatoshi Kiba1, Hisami Yamada1, Shusei Sato2, Tomohiko Kato2, Satoshi Tabata2, Takafumi Yamashino1 and Takeshi Mizuno1,3

1 Laboratory of Molecular Microbiology, School of Agriculture, Nagoya University, Chikusa-ku, Nagoya 464-8601, Japan
2 Kazusa DNA Research Institute, Kazusa, Chiba 292-0812, Japan

Abstract

The Arabidopsis thaliana AHK4 histidine kinase (also known as CRE1 or WOL) acts as a cytokinin signal transducer, presumably, in concert with downstream components, such as histidine-containing phosphotransfer factors (AHPs) and response regulators (ARRs), through the histidine-to-aspartate (His->Asp) phosphorelay. Among 10 members of the type-A ARR family, the cytokinin-induced expression of ARR15 in roots is selectively impaired in the cre1-1 mutant, which carries a mutation in the AHK4 gene, suggesting a link between this type-A response regulator and the AHK4-mediated cytokinin signal transduction in roots. To address this issue further, we characterized a T-DNA insertion mutant of ARR15, and also constructed transgenic lines (referred to as ARR15-ox) that overexpress the ARR15 gene in a manner independent of cytokinin. While the T-DNA insertion mutant (arr15-1) showed no apparent phenotype, the cytokinin-independent overexpression of ARR15 in ARR15-ox plants resulted in a reduced sensitivity toward exogenously applied cytokinin, not only in elongation of roots in plants, but also in green callus formation (or shoot formation) in explants. Cytokinin-induced expressions of certain type-A ARRs were also down-regulated in ARR15-ox plants. These results support the view that ARR15 acts as a repressor that mediates a negative feedback loop in the cytokinin and AHK4-mediated His->Asp phosphorelay.

Footnotes

3 Corresponding author: E-mail, tmizuno{at}agr.nagoya-u.ac.jp; Fax, +81-52-789-4091.


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