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Title 

Mitochondria-associated hexokinases play a role in the control of programmed cell death in Nicotiana benthamiana

Authors 

Moonil KimJ H LimC S AhnK ParkG T KimW T KimH S Pai

Publisher 

American Society of Plant Biologists

Issue Date 

2006

Citation 

Plant Cell, vol. 18, no. 9, pp. 2341-2355

Keywords 

cellsleaf morphologynicotiana benthamianaprogrammed cell death (PCD)arabidopsis proteinATHXK1 protein, Arabidopsisbiological markercaspaseDNA fragmenthexokinase

Abstract 

Recent findings suggest a pivotal role for mitochondria-associated hexokinase in the regulation of apoptosis in animal cells. In this study, virus-induced gene silencing (VIGS) of a hexokinase-encoding Hxk1 caused necrotic lesions on leaves, abnormal leaf morphology, and retarded plant growth in Nicotiana benthamiana. Hxk1 was associated with the mitochondria, and this association required the N-terminal membrane anchor. VIGS of Hxk1 reduced the cellular glucose-phosphorylating activity to ∼31% of control levels without changing the fructose-phosphorylating activity and did not alter hexose phosphate content severely. The affected cells showed programmed cell death (PCD) morphological markers, including nuclear condensation and DNA fragmentation. Similar to animal cell apoptosis, cytochrome c was released into the cytosol and caspase-9- and caspase-3-like proteolytic activities were strongly induced. Furthermore, based on flow cytometry, Arabidopsis thaliana plants overexpressing Arabidopsis HXK1 and HXK2, both of which are predominantly associated with mitochondria, exhibited enhanced resistance to H 2O2- and α-picolinic acid-induced PCD. Finally, the addition of recombinant Hxk1 to mitochondria-enriched fractions prevented H 2O2/clotrimazole-induced cytochrome c release and loss of mitochondria! membrane potential. Together, these results show that hexokinase critically regulates the execution of PCD in plant cells, suggesting a link between glucose metabolism and apoptosis.

ISSN 

1040-4651

Link 

http://dx.doi.org/10.1105/tpc.106.041509

Appears in Collections

1. Journal Articles > Journal Articles

Registered Date

2019-05-02


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