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Plant and Cell Physiology, 1999, Vol. 40, No. 7 733-742
© 1999

Compilation and Characterization of Arabiopsis thaliana Response Regulators Implicated in His-Asp Phosphorelay Signal Transduction

Aya Imamura, Naoto Hanaki, Ayako Nakamura, Tomomi Suzuki, Mitsutaka Taniguchi, Takatoshi Kiba, Chiharu Ueguchi, Tatsuo Sugiyama and Takeshi Mizuno1

Department of Biological Mechanisms and Functions, Graduate School of Bioagricultural Science, Nagoya University Nagoya, 464-8601 Japan

1To whom correspondence should be addressed. E-mail: tmizuno{at}agr.nagoya-u.ac.jp

His-Asp phosphorelays are evolutionary-conserved powerful biological tactics for intracellular signal transduction. Such a phosphorelay is generally made up of "sensor histidine (His)-kinases", "response regulators", and "histidine-containing (HPt) phosphotransmitters". In the higher plant, Arabidopsis thaliana, results from recent intensive studies suggested that His-Asp phosphorelays may be widely used for propagating environmental stimuli, such as phytohormones (e.g., ethylene and cytokinin). In this study, we first inspected extensively the occurrence of Arabidopsis response regulators in order to compile and characterize them. The results showed that this higher plant has, at least, 14 members of the family of response regulators that can be classified into two distinct subtypes (type-A and type-B), as judged from their structural designs, biochemical properties, and expression profiles. Comparative studies were conducted for each representative (ARR3 and ARR4 for type-A, and ARR10 for type-B). It was suggested that expression of the type-A response regulator is cytokinin-inducible, while that of the type-B response regulator appears to be not. Results from yeast two-hybrid analyses suggested that the type-B response regulator may have an ability to stably interact with a set of HPt phosphotransmitters (AHPs). These and other results will be discussed with special reference to the His-Asp phosphorelay signaling network in Arabidopsis thaliana.

(Received March 8, 1999; Accepted May 7, 1999)
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