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ID 32972
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Author
Imai, Akihiro
Hanzawa, Yoshie
Komura, Mio
Yamamoto, Kotaro T.
Komeda, Yoshibumi
Abstract
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 internocle 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.
Keywords
Arabidopsis thaliana
Polyamine
Spermine
Stem elongation
Upstream ORF
Note
Digital Object Identifer:10.1242/dev.02535
Published with permission from the copyright holder. This is the institute's copy, as published in Development, Volume 133, Issue 18, September 2006, Pages 3575-3585.
Publisher URL:http://dx.doi.org/10.1242/dev.02535
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Copyright © 2006 The Company of Biologists Ltd. All rights reserved.
Published Date
2006-09-15
Publication Title
Development
Volume
volume133
Issue
issue18
Publisher
The Company of Biologists
Start Page
3575
End Page
3585
ISSN
0950-1991
NCID
AA10667805
Content Type
Journal Article
language
英語
Copyright Holders
The Company of Biologists
File Version
publisher
Refereed
True
DOI
PubMed ID
Web of Sience KeyUT
Submission Path
biology_general/6