生物谷報(bào)道:新年伊始,,國(guó)際著名雜志《生物化學(xué)》( Journal of Biological Chemistry,283:461-468)發(fā)表了由昆明植物所李唯奇研究員與美國(guó)科學(xué)家合作的論文“Differential degradation of extraplastidic and plastidic lipids during freezing and post-freezing recovery in Arabidopsis Thaliana”,。該研究利用基于ESI-MS/MS的脂類(lèi)組學(xué)方法(Lipidomics),,分析比較了擬南芥在響應(yīng)低溫脅迫的凍和凍融過(guò)程中約120種膜脂分子的組成變化規(guī)律以及磷脂酶D-a1和d在其中的作用。該研究表明,,不同類(lèi)型的膜脂分子或細(xì)胞定位不同的膜脂分子,,在凍害和凍融過(guò)程中發(fā)生不同變化;抑制磷脂酶D-a1和d的表達(dá)對(duì)低溫誘導(dǎo)的磷脂水解產(chǎn)生了不同的作用,。
據(jù)悉,,低溫脅迫是影響植物的生長(zhǎng)發(fā)育、地理分布和作物產(chǎn)量的主要環(huán)境因素,,細(xì)胞膜是植物低溫傷害產(chǎn)生的主要部位,,膜和膜脂分子變化是植物感應(yīng)溫度變化的初始信號(hào)之一。植物響應(yīng)低溫脅迫有三個(gè)不同階段,,即冷馴(cold-acclimation),、冷凍(freezing)和凍融(post-freezing recovery)。
該研究利用組學(xué)方法,,詳細(xì)和有規(guī)模的解析了兩種生態(tài)型和四種基因型的擬南芥膜脂分子在三個(gè)低溫脅迫階段中的變化,,為進(jìn)一步揭示植物響應(yīng)低溫脅迫的機(jī)制提供了重要的基礎(chǔ)。該項(xiàng)研究已被《自然中國(guó)》(Nature China)雜志選為來(lái)自中國(guó)大陸和香港的突出科學(xué)研究成果,,論文的研究亮點(diǎn)已經(jīng)刊登在該雜志的網(wǎng)站上http://www.nature.com/nchina/featured/112007.html
生物谷推薦英文原文:
J. Biol. Chem., Vol. 283, Issue 1, 461-468, January 4, 2008
Differential Degradation of Extraplastidic and Plastidic Lipids during Freezing and Post-freezing Recovery in Arabidopsis thaliana*
Weiqi Li1, Ruiping Wang, Maoyin Li, Lixia Li, Chuanming Wang¶, Ruth Welti||, and Xuemin Wang
From the Kunming Institute of Botany, Chinese Academy of Sciences, 132 Lanhei Road, Kunming 650204, China, the Department of Biology, University of Missouri and Donald Danforth Plant Science Center, St. Louis, Missouri 63121, the ¶Department of Biology, Honghe University, Mengzi, Yunnan 661100, China, and the ||Kansas Lipidomics Research Center, Division of Biology, Kansas State University, Manhattan, Kansas 66506
Changes in membrane lipid composition play important roles in plant adaptation to and survival after freezing. Plant response to cold and freezing involves three distinct phases: cold acclimation, freezing, and post-freezing recovery. Considerable progress has been made toward understanding lipid changes during cold acclimation and freezing, but little is known about lipid alteration during post-freezing recovery. We previously showed that phospholipase D (PLD) is involved in lipid hydrolysis and Arabidopsis thaliana freezing tolerance. This study was undertaken to determine how lipid species change during post-freezing recovery and to determine the effect of two PLDs, PLD1 and PLD, on lipid changes during post-freezing recovery. During post-freezing recovery, hydrolysis of plastidic lipids, monogalactosyldiacylglycerol and plastidic phosphatidylglycerol, is the most prominent change. In contrast, during freezing, hydrolysis of extraplastidic phospholipids, phosphatidylcholine and phosphatidylethanolamine, occurs. Suppression of PLD1 decreased phospholipid hydrolysis and phosphatidic acid production in both the freezing and post-freezing phases, whereas ablation of PLD increased lipid hydrolysis and phosphatidic acid production during post-freezing recovery. Thus, distinctly different changes in lipid hydrolysis occur in freezing and post-freezing recovery. The presence of PLD1 correlates with phospholipid hydrolysis in both freezing and post-freezing phases, whereas the presence of PLD correlates with reduced lipid hydrolysis during post-freezing recovery. These data suggest a negative role for PLD1 and a positive role for PLD in freezing tolerance.
Received for publication, August 13, 2007 , and in revised form, October 24, 2007.
* The work was supported by grants from the United States Department of Agriculture, the Kansas State University (KSU) Plant Biotechnology Center, the National Basic Research Program of China (Grant 2006CB100100), Knowledge Innovation Program of CAS (KSCX2-YW-N-014), NSFC (30670474), NSF (MCB 0455318, IOS 0454866, DBI 0521587, and Kansas NSF EPSCoR award, EPS-0236913), with support from the State of Kansas through the Kansas Technology Enterprise Corporation and KSU, as well from United States Public Health Services Grant P20 RR016475 from the INBRE program of the National Center for Research Resources. The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked "advertisement" in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 To whom correspondence should be addressed. Tel.: 86-871-522-3025; Fax: 86-871-522-3018; E-mail: [email protected] .