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核糖体蛋白 RPL27a 参与分生组织活性和器官发育。

Involvement of ribosomal protein RPL27a in meristem activity and organ development.

机构信息

School of Biological Sciences, The University of Sydney 2006, New South Wales, Australia.

出版信息

Plant Signal Behav. 2011 May;6(5):712-4. doi: 10.4161/psb.6.5.15070. Epub 2011 May 1.

Abstract

The plant shoot apical meristem is established early during embryogenesis and subsequently gives rise to a shoot through reiterative generation of lateral organs and axillary meristems. In our recent manuscript we reported identification and characterization of a semi-dominant mutation in ribosomal protein RPL27a, which disrupts plant growth and shoot development.1 rpl27ac-1d effects on the shoot are evident from an early stage of embryo development. During embryogenesis rpl27-1d mutants are slow growing and are defective in apical patterning with a delay in establishment of the shoot meristem and outgrowth of cotyledons. Concomitant with this disturbed patterning, the shoot meristem genes SHOOT MERISTEMLESS (STM) and CUP-SHAPED COTYLEDON2 (CUC2) are misexpressed in outer cell layers of the rpl27ac-1d embryo and there is a delay in expression of the organ-patterning gene FILAMENTOUS FLOWER (FIL). Genetic interactions between rpl27ac-1d and other ribosomal protein mutants indicates rpl27ac-1d has reduced ribosome function. Our results highlight a role for ribosomal proteins in growth and development and we propose that the ribosome regulates specific patterning events during development.

摘要

植物茎尖分生组织在胚胎发生早期建立,随后通过侧生器官和腋芽分生组织的反复产生来产生茎。在我们最近的手稿中,我们报道了核糖体蛋白 RPL27a 的半显性突变的鉴定和特征,该突变破坏了植物的生长和茎的发育。1 rpl27ac-1d 对茎的影响从胚胎发育的早期阶段就很明显。在胚胎发生过程中,rpl27-1d 突变体生长缓慢,并且在顶端模式形成中存在缺陷,导致茎分生组织的建立和子叶的生长延迟。与这种紊乱的模式形成同时,茎分生组织基因 SHOOT MERISTEMLESS (STM) 和 CUP-SHAPED COTYLEDON2 (CUC2) 在 rpl27ac-1d 胚胎的外层细胞中错误表达,并且器官模式形成基因 FILAMENTOUS FLOWER (FIL) 的表达延迟。rpl27ac-1d 与其他核糖体蛋白突变体之间的遗传相互作用表明 rpl27ac-1d 核糖体功能降低。我们的结果强调了核糖体蛋白在生长和发育中的作用,我们提出核糖体调节发育过程中的特定模式形成事件。

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