首页> 外文OA文献 >The Histidine Kinases CYTOKININ-INDEPENDENT1 and ARABIDOPSIS HISTIDINE KINASE2 and 3 Regulate Vascular Tissue Development in Arabidopsis Shoots[W]
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The Histidine Kinases CYTOKININ-INDEPENDENT1 and ARABIDOPSIS HISTIDINE KINASE2 and 3 Regulate Vascular Tissue Development in Arabidopsis Shoots[W]

机译:组氨酸激酶细胞分裂素-独立1和阿拉伯糖基化组氨酸激酶2和3调节拟南芥芽中血管组织的发育[W]

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摘要

The development and activity of the procambium and cambium, which ensure vascular tissue formation, is critical for overall plant architecture and growth. However, little is known about the molecular factors affecting the activity of vascular meristems and vascular tissue formation. Here, we show that the His kinase CYTOKININ-INDEPENDENT1 (CKI1) and the cytokinin receptors ARABIOPSIS HISTIDINE KINASE2 (AHK2) and AHK3 are important regulators of vascular tissue development in Arabidopsis thaliana shoots. Genetic modifications of CKI1 activity in Arabidopsis cause dysfunction of the two-component signaling pathway and defects in procambial cell maintenance. CKI1 overexpression in protoplasts leads to cytokinin-independent activation of the two-component phosphorelay, and intracellular domains are responsible for the cytokinin-independent activity of CKI1. CKI1 expression is observed in vascular tissues of inflorescence stems, and CKI1 forms homodimers both in vitro and in planta. Loss-of-function ahk2 and ahk3 mutants and plants with reduced levels of endogenous cytokinins show defects in procambium proliferation and an absence of secondary growth. CKI1 overexpression partially rescues ahk2 ahk3 phenotypes in vascular tissue, while the negative mutation CKI1H405Q further accentuates mutant phenotypes. These results indicate that the cytokinin-independent activity of CKI1 and cytokinin-induced AHK2 and AHK3 are important for vascular bundle formation in Arabidopsis.
机译:确保血管组织形成的原菌和形成层的发育和活性对于整个植物的结构和生长至关重要。但是,关于影响血管分生组织和血管组织形成的分子因素知之甚少。在这里,我们显示了His激酶CYTOKININ-INDEPENDENTENT1(CKI1)和细胞分裂素受体ARABIOPSIS HISTIDINE KINASE2(AHK2)和AHK3是拟南芥芽中血管组织发育的重要调节剂。拟南芥中CKI1活性的遗传修饰会导致两组分信号传导途径功能障碍,并引起原菌的细胞维持缺陷。 CKI1在原生质体中的过表达导致两组分磷酸化的细胞分裂素非依赖性激活,而胞内域负责CKI1的细胞分裂素非依赖性活性。在花序茎的血管组织中观察到CKI1表达,并且CKI1在体外和植物中均形成同型二聚体。功能丧失的ahk2和ahk3突变体以及内源性细胞分裂素水平降低的植物在菌斑增殖中存在缺陷,并且没有次级生长。 CKI1过表达可部分挽救血管组织中的ahk2 ahk3表型,而负突变CKI1H405Q则进一步加重了突变表型。这些结果表明,CKI1和细胞分裂素诱导的AHK2和AHK3的细胞分裂素非依赖性活性对于拟南芥中血管束形成很重要。

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