The dwarf phenotype of the Arabidopsis acl5 mutant is suppressed by a mutation in an upstream ORF of a bHLH gene
The dwarf phenotype of the Arabidopsis acl5 mutant is suppressed by a mutation in an upstream ORF of a bHLH gene
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DOI：
10.1242/dev.02535
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发表时间：
2006-09-15
期刊：
影响因子：
4.6
通讯作者：
Takahashi, Taku
中科院分区：
文献类型：
--
作者：
Imai, Akihiro;Hanzawa, Yoshie;Takahashi, Taku
编码精胺合酶的拟南芥 ACAULIS 5 (ACL5) 基因的功能丧失突变体表现出严重的矮化表型。为了阐明 ACL5 介导的茎节间伸长调节途径，我们分离了四种逆转 acl5 矮化表型的无茎抑制子 (sac) 突变体。因为这些突变体不能挽救已知植物激素相关突变体的侏儒症，所以 SAC 基因似乎专门作用于 ACL5 途径。我们鉴定了导致 sac51-d 显性突变体的基因，该突变体几乎完全抑制了 acl5 表型。 sac51-d 破坏 SAC51 的一个短上游开放阅读框 (uORF)，该框编码 bHLH 型转录因子。我们的结果表明，sac51-d 中 uORF 的提前终止导致其自身转录水平增加，这可能是由于主 ORF 翻译增加的结果。我们提出了一个模型，其中 ACL5 在 SAC51 的翻译激活中发挥作用，这可能导致茎伸长所需的基因子集的表达。
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.