4.6 Article

Cytokinin overproduction-caused alteration of flower development is partially mediated by CUC2 and CUC3 in Arabidopsis

期刊

GENE
卷 450, 期 1-2, 页码 109-120

出版社

ELSEVIER SCIENCE BV
DOI: 10.1016/j.gene.2009.11.003

关键词

Arabidopsis; CUC2; CUC3; Cytokinin-responsive genes; Cytokinin signaling; Flower

资金

  1. Ministry of Science and Technology (MOST) of China [2007CB948200]
  2. National Natural Science Foundation (NNSF) of China [30770217]

向作者/读者索取更多资源

Cytokinin is an essential regulator of numerous plant growth and developmental processes. However, less is known about the mechanisms of cytokinin-regulated floral development. In the present study, we found that flower-specific elevation of cytokinin through transgenic expression of an Arabidopsis ATP/ADP isopentenyltransferase 4 (AtIPT4) gene under the control of the APETALA1 (AP1) promoter lead to floral developmental alterations. These changes included promotion of the number of flowers and abnormal development of flowers, which were correlated with enlarged inflorescence and flower meristems. Genome-wide expression profiling revealed that a large number of genes were responsive to increased cytokinin levels, including this first report that the expression of CUP-SHAPED COTYLEDON2 (CUC2) and CUC3 is elevated by cytokinin. Further analysis showed that mutation of cuc2 or cuc3 attenuates the phenotypes ;caused by the AP1: :AtIPT4 transgene. Mutation of the cytokinin receptors Arabidopsis histidine kinase 2 (AHK2) and AHK3 nearly abolished the transgene phenotypes and the enhanced CUC2 and CUC3 transcription induced by cytokinin. Our results indicate that the overproduced cytokinin in flower primordia results in alteration of floral development mainly through AHK2 and AHK3 signaling leading to increased expression of the effector genes CUC2 and CUC3. Thus, it is likely that the CUC2 and CUC3 expression mediated by AHK2 and AHK3 signaling may play roles in regulation of flower development. (C) 2009 Elsevier B.V. All rights reserved.

作者

我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。

评论

主要评分

4.6
评分不足

次要评分

新颖性
-
重要性
-
科学严谨性
-
评价这篇论文

推荐

暂无数据
暂无数据