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DEVELOPMENT AND HORMONE ACTION

CHOTTO1, a Putative Double APETALA2 Repeat Transcription Factor, Is Involved in Abscisic Acid-Mediated Repression of Gibberellin Biosynthesis during Seed Germination in Arabidopsis^1,[W],[OA]

RIKEN Plant Science Center, Yokohama, Kanagawa 230–0045, Japan (R.Y., Y. Kanno, Y.J., K.N., Y. Kamiya, E.N.); and Department of Cell and Systems Biology (E.N.), and Centre for the Analysis of Genome Evolution and Function (E.N.), University of Toronto, Toronto, Ontario, Canada M5S 3B2

The phytohormones abscisic acid (ABA) and gibberellins (GAs) are the primary signals that regulate seed dormancy and germination. In this study, we investigated the role of a double APETALA2 repeat transcription factor, CHOTTO1 (CHO1), in seed dormancy, germination, and phytohormone metabolism of Arabidopsis (Arabidopsis thaliana). Wild-type seeds were dormant when freshly harvested seeds were sown, and these seeds were released from dormancy after a particular period of dry storage (after-ripening). The cho1 mutant seeds germinated easily even in a shorter period of storage than wild-type seeds. The cho1 mutants showed reduced responsiveness to ABA, whereas transgenic plants constitutively expressing CHO1 (p35S::CHO1) showed an opposite phenotype. Notably, after-ripening reduced the ABA responsiveness of the wild type, cho1 mutants, and p35S::CHO1 lines. Hormone profiling demonstrated that after-ripening treatment decreased the levels of ABA and salicylic acid and increased GA₄, jasmonic acid, and isopentenyl adenine when wild-type seeds were imbibed. Expression analysis showed that the transcript levels of genes for ABA and GA metabolism were altered in the wild type by after-ripening. Hormone profiling and expression analyses indicate that cho1 seeds, with a short period of storage, resembled fully after-ripened wild-type seeds. Genetic analysis showed that the cho1 mutation partially restored delayed seed germination and reduced GA biosynthesis activity in the ABA-overaccumulating cyp707a2-1 mutant background but did not restore seed germination in the GA-deficient ga1-3 mutant background. These results indicate that CHO1 acts downstream of ABA to repress GA biosynthesis during seed germination.

² Present address: Department of Plant Breeding and Genetics, Max Planck Institute for Plant Breeding Research, Carl-von-Linné-Weg 10, Cologne 50829, Germany.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Eiji Nambara (eiji.nambara{at}utoronto.ca).

^[W] The online version of this article contains Web-only data.

^[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.142018

^* Corresponding author; e-mail eiji.nambara{at}utoronto.ca.

Received May 24, 2009; accepted July 23, 2009; published July 31, 2009.