PLANT EXPORTIN-T MUTATION DISRUPTS MERISTEM DEVELOPMENT

植物 EXPORTIN-T 突变破坏分生组织发育

• 批准号: 6628751
• 负责人: CHRISTINE A HUNTER
• 金额: $ 2.41万
• 依托单位: UNIVERSITY OF PENNSYLVANIA
• 依托单位国家: 美国
• 财政年份: 2001
• 资助国家: 美国
• 起止时间: 2001-02-01 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/6628751
• 关键词: Arabidopsis; alleles; biological transport; epitope mapping; gene induction /repression; gene mutation; genetically modified plants; in situ hybridization; light microscopy; messenger RNA; molecular cloning; northern blottings; nucleic acid sequence; phenotype; plant genetics; plant growth /development; plant morphology; polymerase chain reaction; protein structure function; regulatory gene; scanning electron microscopy; transfer RNA

Mutations in the Arabidopsis pauses (psd) gene result in the death of undifferentiated cells in the shoot apical meristem, a delay in the production of leaf primordial, and heterochronix shifts in leaf identity. PSD encodes a homologue of exportin-t, a gene required for the nuclear export of mature tRNA molecules. As very few members of the importin/ exportin family have been characterized in multi cellular organisms, several approaches will be taken to understand the role of PSD in Arabidosis development. Specifically: 1) the spatial and temporal requirements for PSD expression will be determined by characterization of the mRNA and protein expression patterns and by targeted expression of the PSD gene, 2) genetic and molecular analysis will be used to assay tRNA export and to determine the effect of the PSD mutation on genes involved in meristern development, leaf initiate, and phase change, and 3) potential downstream factors will be isolated in a screen for enhances and suppressors of the PSD phenotype. These experiments will offer insight into the maintenance and differentiation of pluripotent cells and the regulation of developmental 'clocks.' They will also provide a rare opportunity for the in vivo analysis of nuclear transport machinery during the development of a multi cellular organism.

拟南芥停顿（psd）基因的突变导致茎顶端分生组织中未分化细胞的死亡，延迟叶原基的产生，以及叶身份的异时性转变。PSD编码一个同源的exportin-t，一个基因所需的核输出成熟的tRNA分子。由于在多细胞生物体中很少有输入/输出蛋白家族的成员，因此将采取几种方法来了解PSD在阿拉伯病发展中的作用。具体而言：1）PSD表达的空间和时间要求将通过mRNA和蛋白质表达模式的表征以及PSD基因的靶向表达来确定，2）遗传和分子分析将用于测定tRNA输出并确定PSD突变对涉及分生组织发育、叶起始和相变的基因的影响，和3）在筛选PSD表型的增强子和抑制子中分离潜在的下游因子。这些实验将为多能细胞的维持和分化以及发育时钟的调节提供深入了解。“它们还将为多细胞生物体发育过程中的核运输机制的体内分析提供难得的机会。