Igari Kadunari, Endo Sachiko, Hibara Ken-ichiro, Aida Mitsuhiro, Sakakibara Hitoshi, Kawasaki Tsutomu, Tasaka Masao
Graduate School of Biological Sciences, Nara Institute of Science and Technology, Nara 630-0192, Japan.
Plant J. 2008 Jul;55(1):14-27. doi: 10.1111/j.1365-313X.2008.03466.x.
Possible links between plant defense responses and morphogenesis have been postulated, but their molecular nature remains unknown. Here, we introduce the Arabidopsis semi-dominant mutant uni-1D with morphological defects. UNI encodes a coiled-coil nucleotide-binding leucine-rich-repeat protein that belongs to the disease resistance (R) protein family involved in pathogen recognition. The uni-1D mutation causes the constitutive activation of the protein, which is stabilized by the RAR1 function in a similar way as in other R proteins. The uni-1D mutation induces the upregulation of the Pathogenesis-related gene via the accumulation of salicylic acid, and evokes some of the morphological defects through the accumulation of cytokinin. The rin4 knock-down mutation, which causes the constitutive activation of two R proteins, RPS2 and RPM1, induces an upregulation of cytokinin-responsive genes and morphological defects similar to the uni-1D mutation, indicating that the constitutive activation of some R proteins alters morphogenesis through the cytokinin pathway. From these data, we propose that the modification of the cytokinin pathway might be involved in some R protein-mediated responses.
植物防御反应与形态发生之间可能存在联系，这一点已得到推测，但它们的分子本质仍不清楚。在此，我们介绍具有形态缺陷的拟南芥半显性突变体uni-1D。UNI编码一种卷曲螺旋核苷酸结合富含亮氨酸重复序列蛋白，该蛋白属于参与病原体识别的抗病（R）蛋白家族。uni-1D突变导致该蛋白的组成型激活，其通过RAR1功能以与其他R蛋白类似的方式得以稳定。uni-1D突变通过水杨酸的积累诱导病程相关基因上调，并通过细胞分裂素的积累引发一些形态缺陷。rin4基因敲除突变导致两种R蛋白RPS2和RPM1的组成型激活，诱导细胞分裂素响应基因上调以及与uni-1D突变类似的形态缺陷，表明一些R蛋白的组成型激活通过细胞分裂素途径改变形态发生。基于这些数据，我们提出细胞分裂素途径的修饰可能参与某些R蛋白介导的反应。
