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拟南芥 I 类 KNOTTED 类同源框蛋白在 IDA-HAE/HSL2 花脱落信号通路中作为下游因子发挥作用。

Arabidopsis class I KNOTTED-like homeobox proteins act downstream in the IDA-HAE/HSL2 floral abscission signaling pathway.

机构信息

Department of Molecular Biosciences, University of Oslo, N-0316 Oslo, Norway.

出版信息

Plant Cell. 2011 Jul;23(7):2553-67. doi: 10.1105/tpc.111.084608. Epub 2011 Jul 8.

Abstract

Floral organ abscission in Arabidopsis thaliana is regulated by the putative ligand-receptor system comprising the signaling peptide INFLORESCENCE DEFICIENT IN ABSCISSION (IDA) and the two receptor-like kinases HAESA and HAESA-LIKE2. The IDA signaling pathway presumably activates a MITOGEN-ACTIVATED PROTEIN KINASE (MAPK) cascade to induce separation between abscission zone (AZ) cells. Misexpression of IDA effectuates precocious floral abscission and ectopic cell separation in latent AZ cell regions, which suggests that negative regulators are in place to prevent unrestricted and untimely AZ cell separation. Through a screen for mutations that restore floral organ abscission in ida mutants, we identified three new mutant alleles of the KNOTTED-LIKE HOMEOBOX gene BREVIPEDICELLUS (BP)/KNOTTED-LIKE FROM ARABIDOPSIS THALIANA1 (KNAT1). Here, we show that bp mutants, in addition to shedding their floral organs prematurely, have phenotypic commonalities with plants misexpressing IDA, such as enlarged AZ cells. We propose that BP/KNAT1 inhibits floral organ cell separation by restricting AZ cell size and number and put forward a model whereby IDA signaling suppresses BP/KNAT1, which in turn allows KNAT2 and KNAT6 to induce floral organ abscission.

摘要

拟南芥的花器官脱落由包含信号肽 INFLORESCENCE DEFICIENT IN ABSCISSION(IDA)和两个类受体激酶 HAESA 和 HAESA-LIKE2 的假定配体-受体系统调控。IDA 信号通路可能激活丝裂原激活蛋白激酶(MAPK)级联反应,以诱导离区(AZ)细胞分离。IDA 的异位表达导致过早的花器官脱落和潜在 AZ 细胞区域的异位细胞分离,这表明存在负调控因子以防止 AZ 细胞不受限制和不合时宜的分离。通过筛选恢复 ida 突变体中花器官脱落的突变体,我们鉴定了 KNOTTED-LIKE HOMEOBOX 基因 BREVIPEDICELLUS(BP)/KNOTTED-LIKE FROM ARABIDOPSIS THALIANA1(KNAT1)的三个新突变等位基因。在这里,我们表明 bp 突变体除了过早脱落花器官外,还具有与 IDA 异位表达植物相似的表型共性,如 AZ 细胞增大。我们提出 BP/KNAT1 通过限制 AZ 细胞大小和数量来抑制花器官细胞分离,并提出了一个模型,即 IDA 信号抑制 BP/KNAT1,反过来又允许 KNAT2 和 KNAT6 诱导花器官脱落。

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