The Arabidopsis peptide kiss of death is an inducer of programmed cell death

被引:71
作者
Blanvillain, Robert [2 ]
Young, Bennett [1 ]
Cai, Yao-min [1 ]
Hecht, Valerie [2 ]
Varoquaux, Fabrice [2 ]
Delorme, Valerie [2 ]
Lancelin, Jean-Marc [3 ]
Delseny, Michel [2 ]
Gallois, Patrick [1 ]
机构
[1] Univ Manchester, Fac Life Sci, Manchester M13 9PT, Lancs, England
[2] Univ Perpignan, CNRS UMR 5096, Lab Genome & Dev Plantes, F-66025 Perpignan, France
[3] Univ Lyon 1, CNRS, UMR 5280, Inst Sci Analyt, F-69622 Villeurbanne, France
基金
英国生物技术与生命科学研究理事会;
关键词
BAX inhibitor 1; caspase-like; embryogenesis; p35; HYPERSENSITIVE RESPONSE; PLANT EMBRYOGENESIS; TRACHEARY ELEMENTS; THALIANA; TOBACCO; GENE; OVEREXPRESSION; DEGRADATION; EXPRESSION; ENZYME;
D O I
10.1038/emboj.2011.14
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Programmed cell death (PCD) has a key role in defence and development of all multicellular organisms. In plants, there is a large gap in our knowledge of the molecular machinery involved at the various stages of PCD, especially the early steps. Here, we identify kiss of death (KOD) encoding a 25-amino-acid peptide that activates a PCD pathway in Arabidopsis thaliana. Two mutant alleles of KOD exhibited a reduced PCD of the suspensor, a single file of cells that support embryo development, and a reduced PCD of root hairs after a 55 degrees C heat shock. KOD expression was found to be inducible by biotic and abiotic stresses. Furthermore, KOD expression was sufficient to cause death in leaves or seedlings and to activate caspase-like activities. In addition, KOD-induced PCD required light in leaves and was repressed by the PCD-suppressor genes AtBax inhibitor 1 and p35. KOD expression resulted in depolarization of the mitochondrial membrane, placing KOD above mitochondria dysfunction, an early step in plant PCD. A KOD::GFP fusion, however, localized in the cytosol of cells and not mitochondria. The EMBO Journal (2011) 30, 1173-1183. doi:10.1038/emboj.2011.14; Published online 15 February 2011
引用
收藏
页码:1173 / 1183
页数:11
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