磷脂酸的诱导和降解在植物逆境响应中的作用

磷脂酸(phosphatidic acid,PA)是植物中重要的脂质信号分子,被称为"脂质第二信使",参与多种逆境胁迫相关的信号传导途径.植物体内的PA可通过直接的磷脂酶D途径和间接的磷脂酶C途径产生.当植物受到胁迫刺激后,细胞内的PA含量会在几分钟内升高,在胁迫消失后经磷酸化作用形成甘油二酯焦磷酸降解,恢复到正常水平...     

植物甘油二酯激酶(DGK)信号转导作用

甘油二酯激酶(DGK)是产生信号分子磷脂酸(PA)途径中的一个磷酸激酶,它与磷脂酶C(PLC)协同作用产生PA,磷脂酶D(PLD)途径也是PA产生的一个来源。PA是脂质信号分子,参与调节植物各种细胞生物学过程。文章介绍植物中DGK的信号转导作用、分子生物学反应、DGK的抑制剂以及与底物的亲和力的研究进展。     

植物磷脂酸的特性及其在ABA诱导气孔运动中的作用

磷脂酸(PA)是应答多种生理过程的第二信使, 其作为一个脂质信号快速积累从而响应多种环境。PA主要通过磷脂酶D (PLD)和磷脂酶C/甘油二酯激酶(PLC/DGK)途径产生。基于PLDs的生化特性、激活机制以及在不同类型胁迫下被激活的特定同种型的差异, 不同类型胁迫下会产生特定分子种组成的PA。PA在多种环境下起信号转导作用, 在调节气孔运动中, PA的作用模式主要是通过与多种蛋白结合, 激活或抑制这些蛋白的活性, 进而执行其信使功能。该文主要综述PA的生化特性以及信号途径中PA互作蛋白的研究进展, 并提出PA研究中亟待解决的问题及今后的重点研究方向。     

植物PLC-DGK/PA途径介导的渗透胁迫应答反应

肌醇磷脂依赖的磷脂酶C(PLC)是经典肌醇磷脂信号系统的重要组分,它分解二磷酸磷脂酰肌醇分子(PIP2)产生双信使IP3和DAG分子。动物细胞中DAG激活蛋白激酶C(PKC)参与调节多种细胞功能。植物基因组中缺乏PKC的同源序列,DAG被二酰甘油激酶(DGK)进一步磷酸化形成磷脂酸(PA),形成新的植物特有的第二信使分子。酶蛋白PLC和DGK及其作用的底物和产物形成植物特色的信号途径,该信号途径在植物对非生物和生物胁迫的反应中发挥重要作用。该文从蛋白信号分子的表达特征和脂质信号分子的含量变化等两个方面综述了植物特色的肌醇信号途径PLC-DGK/PA在应答渗透胁迫反应中的作用。除了PLC-DG活性外,PA也可由磷脂酶D(PLD)产生。该文还对两种途径产生的PA进行了讨论。     

磷脂酸和溶血磷脂酸的生理功能

磷脂酸(phosphatidic acid, PA)和溶血磷脂酸(lysophosphatidic acid,LPA)是细胞内和细胞外信号转导的重要磷脂信号分子.它们主要通过磷脂酶D和磷脂酶C两条途径产生,并且PA在磷脂酶A2的催化下可水解生成LPA.越来越多证据表明,PA和LPA在细胞诸多生理功能中起重要作用.本文主要介绍PA和LPA的生理功能及作用机制的研究进展.     

磷脂酸和溶血磷脂酸的生理功能

磷脂酸（phosphatidic acid,PA)和溶血磷脂酸（lysophosphatidic acid,LPA)是细胞内和细胞外信号转导的重要磷脂信号分子。它们主要通过磷脂酶D和磷脂酶C两条途径产生,并且PA在磷脂酶A2的催化下可水解生成LPA。越来越多证据表明,PA和LPA在细胞诸多生理功能中起重要作用。本文主要介绍PA和LPA的生理功能及作用机制的研究进展。     

磷脂酶D信号转导与植物耐盐研究进展

土壤盐害是一个全球性的生态问题,对生态环境和农业生产带来了巨大的负面影响。研究发现,植物磷脂酶D(Phospholipase D,PLD)是磷脂代谢和应答非生物胁迫的重要酶类;PLD具有不同的结构、生化和调节特性,产生信号分子磷脂酸(Phosphatidic acid,PA)并参与多种胁迫反应。总结了PLD及其产物PA调控植物耐盐的相关报道,探讨其感受、应答盐信号的分子机制,为研究植物应答高盐胁迫和农作物分子遗传改良提供相关参考。     

拟南芥中磷脂酶Dδ参与机械伤害诱导的磷脂酸生成（英文）

磷脂酶水解磷脂产生磷脂酸(phosphatidic acid,PA),Dα1和δ是磷脂酶D家族中表达丰度最高的两个成员,已知磷脂酶Dα1参与了机械伤害诱导的磷脂酸信号,但是磷脂酶Dδ是否以及如何参与PA信号尚且未知。本研究利用脂类组学分析方法,比较了拟南芥野生型(WS)和磷脂酶Dδ基因T-DNA插入突变体(PLDδ-KO),在机械伤害后的较长时间段(6 h)的膜脂分子变化。结果发现,机械伤害后,拟南芥两种基因型的大部分膜脂均发生下降,且机械伤害后30 min,PA含量即快速并急剧升高;随着时间的延长,其水平持续升高,直至达到峰值后下降至6 h达到最低值。WS和PLDδ-KO达到PA最高值的时间不同,分别为1 h和3 h;在伤害处理后30 min至3 h期间,PLDδ-KO中的PA水平低于WS,两个基因型中的PA含量最大差值为20%,发生在伤害后1 h。这证明缺失PLDδ基因在一定程度抑制了机械伤害诱导的PA生产,表明PLDδ参与拟南芥响应机械伤害的PA生成,但是其响应较PLDα1作用慢且轻。这是PLDδ响应拟南芥中机械伤害的首次报道。     

植物蛋白磷酸酶2C在非生物胁迫信号通路中的调控作用

植物在非生物胁迫下会产生一系列的形态、生理生化和分子水平上的适应性变化,尤其是非生物胁迫会引起植物体内的蛋白磷酸酶2C(PP2C)基因表达的改变,从而诱导植物合成相关的蛋白以适应胁迫。植物中有不同类型的PP2C亚群,各种PP2C亚群能够通过不同的信号途径参与胁迫应答,因此在植物响应非生物胁迫的过程中发挥重要作用。综述了植物PP2C在非生物胁迫信号通路中的作用机制。     

大鼠脑甘油二酯激酶的活性及其抑制物的研究

<正> 甘油二酯激酶(diacylglycerol kinase,DGK)广泛的存在于动物组织。它在消耗ATP情况下能使甘油二酯(diacylglycerol,DG)转变成磷脂酸(PA),PA再经磷脂酶A_2作用,水解成花生四烯酸,后者是前列腺素合成的原料。 目前已公认DG为第二信使,DG存在于细胞膜上,能特异地激活蛋白激酶C(protein     

Phosphatidic acid: an emerging plant lipid second messenger

Evidence is accumulating that phosphatidic acid is a second messenger. Its level increases within minutes of a wide variety of stress treatments including ethylene, wounding, pathogen elicitors, osmotic and oxidative stress, and abscisic acid. Enhanced signal levels are rapidly attenuated by phosphorylating phosphatidic acid to diacylglycerol pyrophosphate. Phosphatidic acid is the product of two signalling pathways, those of phospholipases C and D, the former in combination with diacylglycerol kinase. Families of these genes are now being cloned from plants. Several downstream targets of phosphatidic acid have been identified, including protein kinases and ion channels.     

Phosphatidic acid: a multifunctional stress signaling lipid in plants

Phosphatidic acid (PA) has only recently been identified as an important signaling molecule in both plants and animals. Nonetheless, it already promises to rival the importance of the classic second messengers Ca(2+) and cAMP. In plants, its formation is triggered in response to various biotic and abiotic stress factors, including pathogen infection, drought, salinity, wounding and cold. In general, PA signal production is fast (minutes) and transient. Recently, our understanding of the role of PA formation in stress responses as a result of phospholipases C and D activity has greatly increased. Moreover, the first protein targets of PA have been identified. Based on this recent work, potential mechanisms by which PA provokes downstream effects are emerging.     

Substrate preference of stress-activated phospholipase D in Chlamydomonas and its contribution to PA formation

In response to various environmental stress conditions, plants rapidly form the intracellular lipid second messenger phosphatidic acid (PA). It can be generated by two independent signalling pathways via phospholipase D (PLD) and via phospholipase C (PLC) in combination with diacylglycerol kinase (DGK). In the green alga Chlamydomonas, the phospholipid substrates for these pathways are characterized by specific fatty acid compositions. This allowed us to establish: (i) PLD's in vivo substrate preference; and (ii) PLD's contribution to PA formation during stress signalling. Accordingly, G-protein activation (1 micro m mastoparan), hyperosmotic stress (150 mm NaCl) and membrane depolarization (50 mm KCl) were used to stimulate PLD, as monitored by the accumulation in 5 min of its unique transphosphatidylation product phosphatidylbutanol (PBut). In each case, PBut's fatty acid composition specifically matched that of phosphatidylethanolamine (PE), identifying this lipid as PLD's favoured substrate. This conclusion was substantiated by analysing the molecular species by electrospray ionization-mass spectrometry (ESI-MS/MS), which revealed that PE and NaCl-induced PBut share a unique (18 : 1)2-structure. The fatty acid composition of PA was much more complex, reflecting the different contributions from the PLC/DGK and PLD pathways. During KCl-induced stress, the PA rise was largely accounted for by PLD activity. In contrast, PLD's contribution to hyperosmotic stress-induced PA was less, being approximately 63% of the total increase. This was because the PLC/DGK pathway was activated as well, resulting in phosphoinositide-specific fatty acids and molecular species in PA.     

Nitric oxide is critical for inducing phosphatidic acid accumulation in xylanase-elicited tomato cells

Nitric Oxide (NO) is a second messenger related to development and (a)biotic stress responses in plants. We have studied the role of NO in signaling during plant defense responses upon xylanase elicitation. Treatment of tomato cell cultures with the fungal elicitor xylanase resulted in a rapid and dose-dependent NO accumulation. We have demonstrated that NO is required for the production of the lipid second messenger phosphatidic acid (PA) via the activation of the phospholipase C (PLC) and diacylglycerol kinase (DGK) pathway. Defense-related responses downstream of PA were studied. PA and, correspondingly, xylanase were shown to induce reactive oxygen species production. Scavenging of NO or inhibition of either the PLC or the DGK enzyme diminished xylanase-induced reactive oxygen species production. Xylanase-induced PLDbeta1 and PR1 mRNA levels decreased when NO or PA production were compromised. Finally, we have shown that NO and PA are involved in the induction of cell death by xylanase. Treatment with NO scavenger cPTIO, PLC inhibitor U73122, or DGK inhibitor R59022 diminished xylanase-induced cell death. On the basis of biochemical and pharmacological experimental results, we have shown that PLC/DGK-derived PA represents a novel downstream component of NO signaling cascade during plant defense.     

Phosphatidic acid production in chitosan-elicited tomato cells, via both phospholipase D and phospholipase C/diacylglycerol kinase, requires nitric oxide

Nitric oxide (NO) and the lipid second messenger phosphatidic acid (PA) are involved in plant defense responses during plant-pathogen interactions. NO has been shown to be involved in the induction of PA production in response to the pathogen associated molecular pattern (PAMP) xylanase in tomato cells. It was shown that NO is critical for PA production induced via phospholipase C (PLC) in concerted action with diacylglycerol kinase (DGK) but not for the xylanase-induced PA via phospholipase D (PLD). In order to study whether this is a general phenomenon during PAMP perception or if it is particular for xylanase, we studied the effect of the PAMP chitosan in tomato cell suspensions. We observed a rapid NO production in tomato cells treated with chitosan. Chitosan induced the formation of PA by activating both PLD and PLC/DGK. The activation of either phospholipase-mediated signaling pathway was inhibited in cells treated with the NO scavenger cPTIO. This indicates that NO is required for PA generation via both the PLD and PLC/DGK pathway during plant defense response in chitosan elicited cells. Responses downstream PA were studied. PLC inhibitors neomycin and U73122 inhibited chitosan-induced ROS production. Differences between xylanase and chitosan-induced phospholipid signaling pathways are discussed.     

Phosphatidic acid plays key roles regulating plant development and stress responses

Phospholipids, including phosphatidic acid(PA),phosphatidylcholine(PC), phosphatidylethanolamine(PE),phosphatidylglycerol(PG), phosphatidylserine(PS) and phosphoinositides, have emerged as an important class of cellular messenger molecules in various cellular and physiological processes, of which PA attracts much attention of researchers. In addition to its effect on stimulating vesicle trafficking, many studies have demonstrated that PA plays a crucial role in various signaling pathways by binding target proteins and regulating their activity and subcellular localization. Here, we summarize the functional mechanisms and target proteins underlying PA-mediated regulation of cellular signaling, development, hormonal responses, and stress responses in plants.