Arabidopsis ERECTA-family receptor kinases mediate morphological alterations stimulated by activation of NB-LRR-type UNI proteins.
Arabidopsis ERECTA-family receptor kinases mediate morphological alterations stimulated by activation of NB-LRR-type UNI proteins.
复制标题
DOI：
10.1093/pcp/pcr032
复制
发表时间：
2011-05
影响因子：
4.9
通讯作者：
N. Uchida;Kadunari Igari;Naomi L. Bogenschutz;K. Torii;M. Tasaka
中科院分区：
文献类型：
--
作者：
N. Uchida;Kadunari Igari;Naomi L. Bogenschutz;K. Torii;M. Tasaka
茎尖分生组织（Shoot apical meriystems, SAMs）和叶腋分生组织（axillary meriystems, AMs）分别在茎尖和叶腋形成分支的过程中起着重要作用。先前，我们发现在拟南芥中，NB-LRR（核苷酸结合位点-富含亮氨酸重复序列）型UNI蛋白的激活通过调节分生组织的调节来影响植物形态。然而，有关参与这一过程的基因的信息仍然缺乏。在这里，我们报道ERECTA （ER）受体激酶家族成员协同介导UNI蛋白激活刺激的形态学改变。UNI - 1d是UNI基因的一个功能获得突变，UNI - 1d突变体表现为花序茎生长的早期终止，并在叶腋形成额外的AMs。前一种缺陷涉及SAM活性的调节，并被er突变抑制。虽然AM表型不受单一er突变的影响，但它受到er家族成员同时突变的抑制。先前的研究表明，反式玉米素（tZ）型细胞分裂素参与了uni-1D突变体的形态表型，并且在uni-1D突变体中，对tZ型细胞分裂素的生物合成至关重要的CYP735A2的表达被调节。我们发现这种CYP735A2表达的调节需要er家族成员的活动。此外，在表达uni的细胞中，ER活性对uni-1D突变体的所有形态表型都有贡献，这表明在uni-1D突变体中观察到的形态学改变中，ER家族依赖性和uni触发的信号通路之间的交叉对话起着重要作用。
Shoot apical meristems (SAMs), which maintain stem cells at the tips of stems, and axillary meristems (AMs), which arise at leaf axils for branch formation, play significant roles in the establishment of plant architecture. Previously, we showed that, in Arabidopsis thaliana, activation of NB-LRR (nucleotide-binding site-leucine-rich repeat)-type UNI proteins affects plant morphology through modulation of the regulation of meristems. However, information about genes involved in the processes was still lacking. Here, we report that ERECTA (ER) receptor kinase family members cooperatively mediate the morphological alterations that are stimulated by activation of UNI proteins. uni-1D is a gain-of-function mutation in the UNI gene and uni-1D mutants exhibit early termination of inflorescence stem growth and also formation of extra AMs at leaf axils. The former defect involves modulation of the SAM activity and is suppressed by er mutation. Though the AM phenotype is not affected by a single er mutation, it is suppressed by simultaneous mutations of ER-family members. It was previously shown that trans-zeatin (tZ)-type cytokinins were involved in the morphological phenotypes of uni-1D mutants and that expression of CYP735A2, which is essential for biosynthesis of tZ-type cytokinins, was modulated in uni-1D mutants. We show that this modulation of CYP735A2 expression requires activities of ER-family members. Moreover, the ER activity in UNI-expressing cells contributes to all morphological phenotypes of uni-1D mutants, suggesting that a cross-talk between ER-family-dependent and UNI-triggered signaling pathways plays a significant role in the morphological alterations observed in uni-1D mutants.