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ASYMMETRIC LEAVES2-LIKE19/LATERAL ORGAN BOUNDARIES DOMAIN30 and ASL20/LBD18 Regulate Tracheary Element Differentiation in Arabidopsis

机译:不对称叶2-LIKE19 /横向器官边界域AIN30和ASL20 / LBD18调节拟南芥气管元素的分化。

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摘要

ASYMMETRIC LEAVES2 (AS2)/LATERAL ORGAN BOUNDARIES DOMAIN (LBD) family proteins are plant-specific nuclear proteins, and genes encoding several family members have been implicated in plant development. We investigated the function of two members of the Arabidopsis thaliana AS2/LBD family, AS2-LIKE19 (ASL19)/LBD30 and ASL20/LBD18, which encode homologous proteins. Both ASL19 and ASL20 were expressed in immature tracheary elements (TEs), and the expression was dependent on VASCULAR-RELATED NAC-DOMAIN PROTEIN6 (VND6) and VND7, which are transcription factors required for TE differentiation. Overexpression of ASL19 and ASL20 induced transdifferentiation of cells from nonvascular tissues into TE-like cells, similar to those induced upon VND6/7 overexpression. By contrast, aberrant TEs were formed when a cDNA encoding a fusion protein of ASL20 with an artificial repressor domain (ASL20-SRDX) was expressed from its native promoter. These results provide evidence that ASL proteins positively regulate TE differentiation. In transgenic plants overexpressing both ASL19 and ASL20, the xylem-deficient phenotype caused by the expression of dominant-negative versions of VND6/7 proteins was not rescued. However, ectopic expression of VND7 was detected in plants overexpressing ASL20. Moreover, VND genes and their downstream targets were downregulated in ASL20-SRDX plants. Therefore, ASL20 appears to be involved in a positive feedback loop for VND7 expression that regulates TE differentiation-related genes.
机译:不对称叶子2(AS2)/横向器官边界域(LBD)家族蛋白是植物特有的核蛋白,编码几个家族成员的基因与植物发育有关。我们调查了拟南芥AS2 / LBD家族的两个成员,AS2-LIKE19(ASL19)/ LBD30和ASL20 / LBD18,其编码同源蛋白的功能。 ASL19和ASL20均在未成熟的气管元件(TEs)中表达,并且表达依赖于与血管相关的NAC域蛋白6(VND6)和VND7,它们是TE分化所需的转录因子。 ASL19和ASL20的过表达诱导了细胞从非血管组织到TE样细胞的转分化,类似于VND6 / 7过表达诱导的细胞分化。相反,当从其天然启动子表达编码具有人工阻遏域的ASL20融合蛋白的cDNA(ASL20-SRDX)时,就会形成异常的TEs。这些结果提供了ASL蛋白正调控TE分化的证据。在过表达ASL19和ASL20的转基因植物中,由VND6 / 7蛋白显性阴性版本的表达引起的木质部缺陷表型无法挽救。但是,在过表达ASL20的植物中检测到VND7的异位表达。此外,在ASL20-SRDX植物中,VND基因及其下游靶标被下调。因此,ASL20似乎参与了调控TE分化相关基因的 VND7 表达的正反馈回路。

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