Kim Moonil, Lee Sanghyeob, Park Kyoungsook, Jeong Eun-Ju, Ryu Choong-Min, Choi Doil, Pai Hyun-Sook
BioNanotechnology Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon 305-333, Republic of Korea.
Biochem Biophys Res Commun. 2006 Apr 7;342(2):514-21. doi: 10.1016/j.bbrc.2006.01.176. Epub 2006 Feb 9.
Programmed cell death (PCD) plays a pivotal role in the elimination of injured or unwanted cells during diverse physiological and developmental conditions in organisms. However in contrast to the animal system, signaling pathways and molecular mechanism of PCD are largely unknown in plants. We previously reported that silencing of NbPAF encoding the alpha6 subunit of 20S proteasome by virus-induced gene silencing activated programmed cell death in plants by inactivating proteasome function. In this study, we analyzed global gene expression profile of PCD induced by suppression of NbPAF expression, in comparison with that of hypersensitive response (HR)-induced PCD, using a cDNA microarray representing 4685 hot pepper genes. HR is a well-characterized PCD program in plants, which occurs in response to pathogen infection. The microarray analyses identified 247 genes whose gene expression was differentially modulated during PCD activated by NbPAF depletion or HR. Most of the genes that were up-regulated during the NbPAF-mediated PCD, including the ubiquitin/proteasome pathway-related genes, were down-regulated during HR cell death. In contrast, transcription of many defense-related genes, transcription factor genes, and photosynthesis-related genes remained unchanged or repressed during NbPAF-mediated PCD, while it was highly induced during HR cell death. Only a small number of genes including antioxidant-related genes and proteases were found to be up-regulated during induction of PCD by both proteasome inactivation and HR. Based on these results, these two PCD pathways appear to be differentially regulated, but some overlapping mechanism exists, which involves core regulators of plant PCD.
程序性细胞死亡(PCD)在生物体不同的生理和发育条件下,对清除受损或不需要的细胞起着关键作用。然而,与动物系统不同,植物中PCD的信号通路和分子机制在很大程度上尚不清楚。我们之前报道,通过病毒诱导的基因沉默使编码20S蛋白酶体α6亚基的NbPAF沉默,会通过使蛋白酶体功能失活而激活植物中的程序性细胞死亡。在本研究中,我们使用代表4685个辣椒基因的cDNA微阵列,分析了NbPAF表达受抑制诱导的PCD的全局基因表达谱,并与过敏反应(HR)诱导的PCD进行了比较。HR是植物中一个特征明确的PCD程序,它在对病原体感染的反应中发生。微阵列分析鉴定出247个基因,其基因表达在由NbPAF缺失或HR激活的PCD过程中受到差异调节。在NbPAF介导的PCD过程中上调的大多数基因,包括泛素/蛋白酶体途径相关基因,在HR细胞死亡过程中下调。相反,许多防御相关基因、转录因子基因和光合作用相关基因的转录在NbPAF介导的PCD过程中保持不变或受到抑制,而在HR细胞死亡过程中则被高度诱导。在蛋白酶体失活和HR诱导的PCD过程中,仅发现少数基因(包括抗氧化相关基因和蛋白酶)上调。基于这些结果,这两种PCD途径似乎受到差异调节,但存在一些重叠机制,其中涉及植物PCD的核心调节因子。