Abstract

In Arabidopsis thaliana, a number of circadian-associated factors have been identified, including TOC1 (TIMING OF CAB EXPRESSION1) that is believed to be a component of the central oscillator. TOC1 is a member of a small family of proteins, designated as ARABIDOPSIS PSEUDO-RESPONSE REGULATORS (APRR1/TOC1, APRR3, APRR5, APRR7, and APRR9). As demonstrated previously, these APRR1/TOC1 quintet members are crucial for a better understanding of the molecular links between circadian rhythms and photosensory signal transduction. Here we focused on the light-induced quintet member, APRR9, and three critical issues with regard to this member were simultaneously addressed: (i) clarification of the mechanism underlying the light-dependent acute response of APRR9, (ii) clarification of the phenotype of a null mutant of APRR9, (iii) identification of protein(s) that interacts with APRR9. In this study, we present the results that support the following views. (i) A phytochrome-mediated signaling pathway(s) activates the transcription of APRR9, leading to the acute light response of APRR9. (ii) The severe mutational lesion of APRR9 singly, if not directly, affects the period (and/or phase) of free-running rhythms, in continuous light, of every circadian-controlled gene tested, including the clock genes, APRR1/TOC1, CCA1, and LHY. (iii) The APRR9 protein is capable of interacting with APRR1/TOC1, suggesting a hetrodimer formation between these cognate family members. These results are discussed within the context of a current consistent model of the Arabidopsis circadian oscillator.

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