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Overexpression of miR165 Affects Apical Meristem Formation, Organ Polarity Establishment and Vascular Development in Arabidopsis

机译:miR165的过表达影响拟南芥根分生组织的形成,器官极性的建立和血管的发育。

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The class III homeodomain leucine-zipper (HD-ZIP III) genes are thought to be targets of microRNAs (miRNAs) 165 and 166, but it is not known whether all the developmental processes affected by mutations of the HD-ZIP III genes could be recapitulated by an alteration in the expression of miR165 and miR166. Previous work showed that overexpression of miR166 by activation tagging results in down-regulation of the ATHB-9/PHV, ATHB-14/PHB and ATHB-15 genes, and concomitantly causes an enlargement of shoot apical meristems (SAMs) and an enhancement in vascular development. Here we demonstrated that overexpression of miR165 causes a drastic reduction in the transcript levels of all five HD-ZIP III genes in Arabidopsis. The miR165 overexpressors display prominent phenotypes reminiscent of loss-of-function mutants of rev phb phv and rev/ifl1, including loss of SAM, alteration of organ polarity, abnormal formation of carpels, inhibition of vascular development and aberrant differentiation of interfascicular fibers. Global gene expression analysis revealed a link between miR165 overexpression and altered expression of genes involved in auxin signaling and vascular development. Our results demonstrate that overexpression of miR165 recapitulates the phenotypes caused by loss-of-function mutations of HD-ZIP III genes, such as loss of SAM, altered organ polarity and defects in development of vascular tissues and interfascicular fibers.
机译:III类同源域亮氨酸拉链(HD-ZIP III)基因被认为是microRNA(miRNA)165和166的靶标,但尚不清楚是否所有受HD-ZIP III基因突变影响的发育过程都可能是通过miR165和miR166表达的改变来概括。先前的工作表明,通过激活标签过度表达miR166会导致ATHB-9 / PHV,ATHB-14 / PHB和ATHB-15基因的下调,并同时导致茎尖分生组织(SAMs)增大和增强。血管发育。在这里,我们证明了miR165的过表达导致拟南芥中所有五个HD-ZIP III基因的转录水平急剧降低。 miR165过表达子表现出显着的表型,使人想起rev phb phv和rev / ifl1的功能丧失突变体,包括SAM丧失,器官极性改变,心皮异常形成,血管发育抑制和束间纤维异常分化。全局基因表达分析揭示了miR165过表达与生长素信号传导和血管发育相关基因表达的改变之间的联系。我们的结果表明,miR165的过表达概括了HD-ZIP III基因功能缺失突变(例如SAM缺失,器官极性改变以及血管组织和束间纤维发育缺陷)引起的表型。

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