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First published online August 25, 2006
doi: 10.1242/10.1242/dev.02535

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The dwarf phenotype of the Arabidopsis acl5 mutant is suppressed by a mutation in an upstream ORF of a bHLH gene

Akihiro Imai^1,2, Yoshie Hanzawa^2,*, Mio Komura^1,2, Kotaro T. Yamamoto², Yoshibumi Komeda^2, and Taku Takahashi^1,

¹ Division of Bioscience, Graduate School of Natural Science and Technology, Okayama University, Okayama 700-8530, Japan.
² Division of Biological Sciences, Graduate School of Science, Hokkaido University, N10, W8, Sapporo 060-0810, Japan.

Author for correspondence (e-mail: perfect{at}cc.okayama-u.ac.jp)

Accepted 17 July 2006

Loss-of-function mutants of the Arabidopsis thaliana ACAULIS 5 (ACL5) gene, which encodes spermine synthase, exhibit a severe dwarf phenotype. To elucidate the ACL5-mediated regulatory pathways of stem internode elongation, we isolated four suppressor of acaulis (sac) mutants that reverse the acl5 dwarf phenotype. Because these mutants do not rescue the dwarfism of known phytohormone-related mutants, the SAC genes appear to act specifically on the ACL5 pathways. We identify the gene responsible for the dominant sac51-d mutant, which almost completely suppresses the acl5 phenotype. sac51-d disrupts a short upstream open reading frame (uORF) of SAC51, which encodes a bHLH-type transcription factor. Our results indicate that premature termination of the uORF in sac51-d results in an increase in its own transcript level, probably as a result of an increased translation of the main ORF. We suggest a model in which ACL5 plays a role in the translational activation of SAC51, which may lead to the expression of a subset of genes required for stem elongation.

Key words: Arabidopsis thaliana, Polyamine, Spermine, Stem elongation, Upstream ORF

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