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UDP-Glucose Pyrophosphorylase Is a Novel Plant Cell Death Regulator
被引:30
|作者:
Chivasa, Stephen
[1
]
Tome, Daniel F. A.
[1
,2
]
Slabas, Antoni R.
[1
]
机构:
[1] Univ Durham, Sch Biol & Biomed Sci, Durham DH1 3LE, England
[2] Univ Warwick, Sch Life Sci, Warwick CV4 7AL, England
基金:
英国生物技术与生命科学研究理事会;
关键词:
fumonisin;
sucrose;
UDP-glucose pyrophosphorylase;
proteomics;
cell death;
MITOCHONDRIAL PERMEABILITY TRANSITION;
SALICYLIC-ACID;
HYPERSENSITIVE RESPONSE;
ARABIDOPSIS-THALIANA;
CARBONIC-ANHYDRASE;
DISEASE RESISTANCE;
SUCROSE SYNTHASE;
DEFENSE;
GENE;
PROTEIN;
D O I:
10.1021/pr3010887
中图分类号:
Q5 [生物化学];
学科分类号:
071010 ;
081704 ;
摘要:
Programmed cell death (PCD) is an essential process that functions in plant organ sculpture, tissue differentiation, nutrient recycling, and defense against pathogen attack A full understanding of the mechanism of PCD in plants is hindered by the limited identification of protein components of the complex signaling circuitry that underpins this important physiological process. Here we have used Arabidopsis thaliana and fumonisin B1 (FB1) to identify proteins that constitute part of the PCD signaling network We made an inadvertent, but important observation that exogenous sucrose modulates FBI-induced cell death and identified sucrose-induced genes from publicly available transcriptomic data sets for reverse genetic analyses. Using transfer-DNA gene knockout plants, UDP-glucose pyrophosphorylase 1 (UGP1), a sucrose-induced gene, was demonstrated to be a critical factor that regulates FB1-induced PCD. We employed 2D-DiGE to identify proteomic changes preceding PCD after exposure of Arabidopsis to FB1 and used UGP1 knockout plants to refine the analysis and isolate downstream candidate proteins with a putative PCD regulatory function. Our results reveal chloroplasts as the predominantly essential organelles in FB1-induced PCD. Overall, this study reveals a novel function of UGP1 as a cell death regulator and provides candidate proteins likely recruited downstream in the activation of plant PCD.
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页码:1743 / 1753
页数:11
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