Mitochondrial proteome during salt stress-induced programmed cell death in rice.
It has been shown that mitochondria play a pivotal role in plant programmed cell death (PCD). Previous study established a salt stress-induced PCD model in rice (Oryza sativa L. cv. WYJ 8th) root tip cells, demonstrated by DNA laddering, cytochrome c release, and TUNEL positive reaction. In this study, the role of mitochondria during the early phase of PCD (2h-PCD) was analyzed in rice roots. After 2h-PCD induction, the integrity of mitochondria decreased slightly, consistent with a small release of cytochrome c. 2h-PCD partially inhibited electron transport, resulting in oxidative burst in mitochondria. However, ATP production maintained constant. Mitochondria proteome were analyzed by two-dimensional IEF/SDS-PAGE before and after 2h-PCD induction, and eight PCD-related proteins were identified. Among them, four proteins were up-regulated after PCD induction, which included glycoside hydrolase, mitochondrial heat shock protein 70, 20S proteasome subunit, and Cu/Zn-superoxide dismutase, and four were down-regulated, namely ATP synthase beta subunit, cytochrome c oxidase subunit 6b, S-adenosylmethionine synthetase 2, and transcription initiation factor eIF-3 epsilon. These results suggested that ATP synthase may not be the major producer of ATP in mitochondria during the early stage of PCD in rice. Glycoside hydrolase may be involved in ETC impairment and ROS burst, and mitochondrial HSP70 is a potential candidate for PCD regulation. The possible roles of other proteins on PCD initiation were also discussed.
Chen
Xi
X
Department of Biochemistry and Molecular Biology, Nanjing Agricultural University, Weigang, China.
Wang
Ying
Y
Li
Jianyou
J
Jiang
Ailiang
A
Cheng
Yanwei
Y
Zhang
Wei
W
D000255:Adenosine Triphosphate / Q000378:metabolism; D017209:Apoptosis / Q000187:drug effects*; D003576:Electron Transport Complex IV / Q000235:genetics / Q000378:metabolism; D015180:Electrophoresis, Gel, Two-Dimensional; D004591:Electrophoresis, Polyacrylamide Gel; D039621:Eukaryotic Initiation Factor-3 / Q000235:genetics / Q000378:metabolism; D006026:Glycoside Hydrolases / Q000235:genetics / Q000378:metabolism; D018840:HSP70 Heat-Shock Proteins / Q000235:genetics / Q000378:metabolism; D006861:Hydrogen Peroxide / Q000378:metabolism; D015151:Immunoblotting; D018519:Meristem / Q000166:cytology / Q000378:metabolism / Q000648:ultrastructure; D008716:Methionine Adenosyltransferase / Q000235:genetics / Q000378:metabolism; D008854:Microscopy, Electron; D024101:Mitochondrial Proteins / Q000032:analysis / Q000235:genetics / Q000378:metabolism*; D025261:Mitochondrial Proton-Translocating ATPases / Q000235:genetics / Q000378:metabolism; D012275:Oryza / Q000166:cytology / Q000187:drug effects* / Q000378:metabolism; D010940:Plant Proteins / Q000235:genetics / Q000378:metabolism; D018517:Plant Roots / Q000166:cytology / Q000187:drug effects / Q000378:metabolism; D020543:Proteome / Q000032:analysis / Q000378:metabolism; D017382:Reactive Oxygen Species / Q000378:metabolism; D020133:Reverse Transcriptase Polymerase Chain Reaction; D012965:Sodium Chloride / Q000494:pharmacology*; D019032:Spectrometry, Mass, Matrix-Assisted Laser Desorption-Ionization; D013482:Superoxide Dismutase / Q000235:genetics / Q000378:metabolism; D013997:Time Factors
D039621:Eukaryotic Initiation Factor-3; D018840:HSP70 Heat-Shock Proteins; D024101:Mitochondrial Proteins; D010940:Plant Proteins; D020543:Proteome; D017382:Reactive Oxygen Species; D012965:Sodium Chloride; D000255:Adenosine Triphosphate; D006861:Hydrogen Peroxide; D013482:Superoxide Dismutase; D003576:Electron Transport Complex IV; D008716:Methionine Adenosyltransferase; D006026:Glycoside Hydrolases; D025261:Mitochondrial Proton-Translocating ATPases