The Arabidopsis STV1 protein, responsible for translation reinitiation, is required for auxin-mediated gynoecium patterning
The Arabidopsis STV1 protein, responsible for translation reinitiation, is required for auxin-mediated gynoecium patterning
复制标题
DOI：
10.1105/tpc.105.036533
复制
发表时间：
2005-11-01
期刊：
影响因子：
11.6
通讯作者：
Okada, K
中科院分区：
文献类型：
--
作者：
Nishimura, T;Wada, T;Okada, K
核糖体蛋白L24 （RPL24）参与多顺反子基因的翻译再启动。一个新分离的拟南芥短阀1 （stv1）突变体，其中一个rpl24编码基因RPL24B被删除，除了核糖体缺乏引起的表型外，还显示出雌蕊顶端-基部模式的特定缺陷。类似的雌蕊表型是由生长素反应因子（ARF）基因ETTIN （ETT）和MONOPTEROS （MP）的突变引起的，这两个基因在其5'-转录先导序列中具有上游开放阅读框（uorf）。stv1双突变体和弱ett突变等位基因的雌蕊与强ett等位基因的雌蕊相似，用消除uorf的ett构建体进行转化，部分抑制了stv1的雌蕊表型，这表明stv1可能通过其uorf影响ett翻译。对5'-leader-报告基因融合的分析表明，ETT和MP的uorf负向调节下游主要orf的翻译，表明翻译重启动是这些蛋白表达的重要步骤。综上所述，我们认为ARF转录本的翻译重新启动的扰动导致了在stv1突变体中观察到的雌蕊图案缺陷。
Ribosomal protein L24 (RPL24) is implicated in translation reinitiation of polycistronic genes. A newly isolated Arabidopsis thaliana short valve1 (stv1) mutant, in which one of the RPL24-encoding genes, RPL24B, is deleted, shows specific defects in the apical-basal patterning of the gynoecium, in addition to phenotypes induced by ribosome deficiency. A similar gynoecium phenotype is caused by mutations in the auxin response factor (ARF) genes ETTIN (ETT) and MONOPTEROS (MP), which have upstream open reading frames (uORFs) in their 5'-transcript leader sequences. Gynoecia of a double mutant of stv1 and a weak ett mutant allele are similar to those of a strong ett allele, and transformation with a uORF-eliminated ETT construct partially suppressed the stv1 gynoecium phenotype, implying that STV1 could influence ETT translation through its uORFs. Analyses of 5'-leader-reporter gene fusions showed that the uORFs of ETT and MP negatively regulate the translation of the downstream major ORFs, indicating that translation reinitiation is an important step for the expression of these proteins. Taken together, we propose that perturbation of translation reinitiation of the ARF transcripts causes the defects in gynoecium patterning observed in the stv1 mutant.