Misexpression of the cyclin-dependent kinase inhibitor ICK1/KRP1 in single-celled Arabidopsis trichomes reduces endoreduplication and cell size and induces cell death
Misexpression of the cyclin-dependent kinase inhibitor ICK1/KRP1 in single-celled Arabidopsis trichomes reduces endoreduplication and cell size and induces cell death
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DOI：
10.1105/tpc.008342
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发表时间：
2003-02-01
期刊：
影响因子：
11.6
通讯作者：
Hülskamp, M
中科院分区：
文献类型：
--
作者：
Schnittger, A;Weinl, C;Hülskamp, M
在许多植物细胞类型中，细胞大小和DNA含量之间存在正相关关系。相反，显性负周期蛋白依赖性蛋白(CDK)或CDK抑制蛋白(ick/krps)在拟南芥和烟草叶片中的错误表达揭示了细胞生长可以与细胞周期进程和DNA含量解偶联。然而，细胞生长似乎也是以非细胞自主的方式受到器官大小的控制，这使得在普遍存在的表达分析中很难判断假定的细胞生长调节因子的细胞自主功能。在这里，我们以拟南芥毛状体为模型系统，研究了CDK抑制剂ICK1/KRP1对细胞生长和分化的作用，而不受器官背景的任何补偿影响。通过分析细胞大小与DNA含量的关系，我们剖析了细胞在DNA依赖和DNA非依赖过程中的生长。我们进一步发现，ICK1/KRP1的错误表达干扰了植物的分化和诱导细胞死亡，将细胞周期进展、分化和细胞死亡联系在一起。在植物中，ICK1/KRP1的功能依赖于C-末端结构域，并受N-末端结构域的负调控。最后，我们确定CDKA；1和D型细胞周期蛋白是ICK1/KRP1在体内表达的可能靶点。
A positive correlation between cell size and DNA content has been recognized in many plant cell types. Conversely, misexpression of a dominant-negative cyclin-dependent kinase (CDK) or CDK inhibitor proteins (ICK/KRPs) in Arabidopsis and tobacco leaves has revealed that cell growth can be uncoupled from cell cycle progression and DNA content. However, cell growth also appears to be controlled in a non-cell-autonomous manner by organ size, making it difficult in a ubiquitous expression assay to judge the cell-autonomous function of putative cell growth regulators. Here, we investigated the function of the CDK inhibitor ICK1/KRP1 on cell growth and differentiation independent of any compensatory influence of an organ context using Arabidopsis trichomes as a model system. By analyzing cell size with respect to DNA content, we dissected cell growth in a DNA-dependent and a DNA-independent process. We further found that ICK1/KRP1 misexpression interfered with differentiation and induced cell death, linking cell cycle progression, differentiation, and cell death in plants. The function of ICK1/KRP1 in planta was found to be dependent on a C-terminal domain and regulated negatively by an N-terminal domain. Finally, we identified CDKA;1 and a D-type cyclin as possible targets of ICK1/KRP1 expression in vivo.