| Budget Amount *help |
¥15,000,000 (Direct Cost: ¥15,000,000)
Fiscal Year 2006: ¥3,400,000 (Direct Cost: ¥3,400,000)
Fiscal Year 2005: ¥5,100,000 (Direct Cost: ¥5,100,000)
Fiscal Year 2004: ¥6,500,000 (Direct Cost: ¥6,500,000)
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| Research Abstract |
Cytokinins are perceived in Arabidopsis by the three sensor histidine kinases (CRE1 etc.), and activate the transcription-factor type (B-type) response regulators such as ARR1. Therefore, ARR1 seemed to be functionally located downstream of CRE1. This was confirmed by the fact that ARR1 activation suppresses the defects of CRE1 in the absence of cytokinin. Biochemical study in vitro showed that CRE1 is capable of autophosphorylation followed by transfer of its phosphoryl group to ARR1 via HPt intervening factors (AHPs), mimicking prokaryotic His-Asp phosphorelay. We searched, in a genome-wide scale, genes targeted directly by ARR1, and identified various genes that code for A-type response regulators, transcription factors, cytokinin-catabolising enzymes, and pathogen-wounding response proteins. The majority of these identified targets were genes whose expression are immediately and primarily induced by cytokinin. Contribution of ARR1 to the respective target genes varied significantly, indicating that the B-type response regulators are functionally overlapping with each other but have some preference for the respective target genes. These results implied that the majority of immediately and primarily cytokinin-responsive genes are activated by the His-Asp phosphorelay system consisting of CRE1 and ARR1, and that no other regulatory system is involved in cytokinin signaling in Arabidopsis. Furthermore, suppression experiments of CRE1 defects led to the identification of a pseudo-AHP gene (AHP6). AHP6 contributed toward the regulation of cell fate during root vascular development by inhibiting cytokinin signaling. Since this inhibition is thought to occur by competing with AHPs, the view of AHP intervention between CRE1 and ARR1 was further strengthened in vivo.
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