褪黑素对谷氨酸致痫大鼠海马cAMP水平的影响

目的探讨褪黑素(melatonin, MT)对谷氨酸(glutamate,Glu)致痫大鼠海马cAMP水平的影响.方法　随机将健康SD雄性大鼠分为A、B、C、D 4组,每组10只,分别为对照组、Glu组、MT Glu组和Luzidole MT Glu组,观察并记录动物行为学及EEG改变,应用放射免疫方法检测各组动物脑内cAMP水平.结果行为学观察和EEG显示,B组和D组大鼠均出现痫性发作,并出现频发性痫性放电,C组大鼠痫性发作不明显,无频发性痫性放电出现;放射免疫分析结果显示,B组和D组海马cAMP含量均较对照组显著的升高(P<0.05);C组较B组和D组cAMP水平明显降低(P<0.05),与A组无明显差异性(P>0.05).结论MT对Glu致痫大鼠有抑痫作用,此作用是通过其受体调节海马内cAMP水平来实现的.     

氯喹对戊四氮致痫大鼠皮质和海马谷氨酸和NMDAR1表达的影响

目的观察氯喹对戊四氮致痫大鼠皮质和海马谷氨酸(glutamate,Glu)和N-甲基-D-天冬氨酸受体1(NMDAR1,NR1)表达的影响,探讨氯喹在癫痫发生发展过程中对神经递质传导的作用。方法48只健康雄性SD大鼠随机分为对照组(12只)、戊四氮致痫组(60mg/kg,i.p.,18只)和氯喹干预组(0.61mg/kg,i.c.v.,18只)。每组分6个时间点:1h、2h、4h、8h、12h和24h。观察大鼠行为表现和脑电图改变,用免疫组化检测大鼠皮质和海马Glu和NR1的变化。结果对照组无痫样发作,戊四氮致痫组有重型的痫样发作(Ⅲ-Ⅴ级),氯喹干预组有轻型的痫样发作(Ⅰ-Ⅲ级)(P<0.05);戊四氮致痫组脑电记录呈频发高幅的痫样波,氯喹干预组痫样波幅低且缓;Glu和NR1在戊四氮致痫组表达强,以海马为著,与对照组比较有显著性差异(P<0.05),氯喹干预组与对照组比较无显著性差异(P>0.05)。结论氯喹通过对戊四氮致痫大鼠皮质和海马神经递质Glu和NR1信号传导通路的抑制作用,影响致痫大鼠痫样发作的发生和发展。     

褪黑素对谷氨酸致痫大鼠海马内谷氨酸、GABA及其受体水平的影响

目的探讨褪黑素(melatonin,MT)对谷氨酸(glutamate,Glu)致痫大鼠海马内Glu及GluR2、γ-氨基丁酸(γ-aminobutyric-acid,GABA)及其受体GABRA1水平的影响,进而研究褪黑素的抑痫作用机制。方法随机将健康SD雄性大鼠40只分为A、B、C、D组,每组10只。A组:生理盐水组;B组:MT Glu组;C组:Glu致痫组;D组:Luzidole MT Glu组。观察并记录行为学变化,采用免疫组化法进行Glu、GluR2、GABA和GABRA1免疫组化染色和图像分析。结果行为学观察结果显示,C组和D组大鼠均有不同程度的癫痫发作,B组大鼠癫痫发作不明显,A组无发作;免疫组化结果显示,C组和D组海马内CA1-CA3区和齿状回Glu阳性反应较A组增强(P<0.05),GluR2、GABA和GABRA1均较A组减弱(P<0.05),B组Glu较C组和D组阳性反应有显著性减弱(P<0.05),GluR2、GABA和GABRA1阳性反应均较C组和D组有显著性增强(P<0.05),而B组与A组无明显差异性。结论MT通过增加GABA及其受体GABRA1和GluR2的作用和抑制Glu作用对Glu致痫大鼠癫痫发作发挥抑制作用。     

氯喹对戊四氮致痫大鼠皮质和海马白细胞介素1β及肿瘤坏死因子α表达的影响

目的观察氯喹对戊四氮致痫大鼠皮质和海马白细胞介素1β(IL-1β)及肿瘤坏死因子α(TNF-α)表达的影响,探讨其在癫痫发生发展过程中的作用.方法 48只健康雄性SD大鼠随机分为对照组(12只)、戊四氮(PTZ)致痫组(18只,60mg/kg,i.p.)和氯喹干预组(18只,氯喹0.61mg/kg,i.c.v.,2h后注射PTZ).每组确定6个时间点:1h、2h、4h、8h、12h和24h.观察大鼠行为表现,记录脑电改变,用免疫组化检测皮质和海马IL-1β和TNF-α表达的变化.结果对照组无痫样发作和痫样放电,戊四氮致痫组痫样发作重(Ⅲ-Ⅴ级),氯喹干预组轻(Ⅰ-Ⅲ级)(P<0.05);脑电记录显示戊四氮致痫组呈频发高幅的痫样波,氯喹干预组痫样波幅低且缓;LI-1β和TNF-α在戊四氮致痫组皮质和海马表达强,与对照组比较差异有显著性(P<0.05),氯喹干预组与对照组比较差异无显著性(P>0.05).结论氯喹可能通过对IL-1β和TNF-α表达的抑制减轻戊四氮致痫大鼠的痫样放电和痫样发作程度.这些结果提示,氯喹在防治癫痫方面可能是理想的抗痫剂.     

褪黑素对马桑内酯致痫大鼠海马内SP水平的影响

目的探讨褪黑素（melatonin,MT）对马桑内酯致痫大鼠海马内P物质水平的影响,以探讨褪黑素的抑痫作用机制。方法随机将健康成年雄性SD大鼠40只分为A、B、C、D 4组,每组10只。A组：生理盐水组;B组：马桑内酯组;C组：褪黑素＋马桑内酯组;D组：Luzindole＋褪黑素＋马桑内酯组。观察并记录行为学变化,然后分别采用免疫组织化学方法进行SP免疫组织化学染色,实时荧光定量PCR方法检测海马内SP mRNA含量变化。结果B组和D组大鼠均有不同程度的癫痫发作,而C组大鼠癫痫发作不明显,A组几乎均无发作;免疫组化结果显示,四组大鼠海马各区均有SP免疫反应阳性神经元,B组、D组与A组、C组比海马内SP免疫阳性反应明显增强（P〈0.05）,而A组与C组比无明显差异（P〉0.05）;RT-PCR结果提示,B组、D组与A组、C组相比,大鼠海马内SP mRNA明显升高（P〈0.05）,而A组与C组比无明显差异（P〉0.05）。结论MT能通过下调海马内SP水平抑制癫痫发作。     

电针和7-硝基吲唑对癫痫的效应及其与脑内一氧化氮的关系

为进一步探索ＮＯ在癫痫诱导和发作以及针刺抗痫中的作用,本文采用特异性ｎＯＳ阻断剂７－硝基吲唑（７－ＮＩ）观察ＮＯ合成减少时青霉素致痫的诱导和发作的变化,并使用ＮＯ敏感电极实时连续记录青霉致痫及穴位针刺和注射７－ＮＩ时大鼠海马内ＮＯ的变化。结果表明,癫痫使发作脑电总功率剧烈升高。穴位针刺后发作明显减弱,各时间点脑电总功率与青霉素注射时有显著差别。７－ＮＩ使诱发时间缩短,阈值降低,但发作程度减轻,在各     

褪黑素对谷氨酸钠致痫大鼠脑内一氧化氮含量的影响

目的观察褪黑素(Melatonin,MT)对谷氨酸钠致痫大鼠脑内一氧化氮(nitric oxide,NO)含量的影响,研究其抑制癫痫的作用机制。方法40只健康雄性SD大鼠随机分为4组(每组10只):生理盐水对照组(NS组);谷氨酸钠致痫组(Glu组);褪黑素+谷氨酸钠组(MT+Glu组);Luzidole+褪黑素+谷氨酸组(Luz+MT+Glu组)。观察大鼠行为变化,记录脑电图,用NADPH组织化学反应检测大鼠海马内NO含量变化。结果行为学观察和EEG显示,NS组无痫样发作和痫样放电,Glu组和Luz+MT+Glu组痫样发作重(Ⅲ-Ⅴ级),脑电图显示频发高幅的痫样波,MT+Glu组有轻微发作(0-Ⅱ级),脑电图上偶见散在单个微小痫样波;NADPH组织化学反应结果显示,Glu组和Luz+MT+Glu组大鼠大脑皮质及海马内NOS阳性细胞与对照组比较增多,差异性明显(P<0.05),MT+Glu组较Glu组和Luz+MT+Glu组内NOS阳性细胞减少,差异性明显(P<0.05)。结论MT对谷氨酸钠致痫大鼠痫样发作程度、痫样放电有抑制作用,其机制之一是经其特异性受体,减弱NO作用,进而发挥抑痫效应。     

褪黑素对谷氨酸钠致痫大鼠海马5-羟色胺水平的影响

目的观察褪黑素(Melatonin,MT)对谷氨酸钠(Glutamate,Glu)致痫大鼠海马5-羟色胺(5-hydroxytryptamine,5-HT)水平的影响,研究其抑制癫痫的作用机制。方法40只健康雄性SD大鼠随机分为4组(每组10只),分别为生理盐水对照组(NS组);谷氨酸钠致痫组(Glu组);褪黑素 谷氨酸钠组(MT Glu组);Luzidole 褪黑素 谷氨酸钠组(Luz MT Glu组)。观察并记录大鼠行为学及脑电图改变,用免疫组织化学方法检测大鼠海马内5-HT含量变化。结果行为学观察和EEG显示,NS组无痫样发作和痫样放电,Glu组和Luz MT Glu组痫样发作重(Ⅲ-Ⅴ级),脑电图显示频发高幅的痫样波,TM Glu组无或仅有轻微发作(0-Ⅱ级),脑电图上无或偶见散在单个微小痫样波;免疫组织化学分析结果显示,Glu组和Luz MT Glu组大鼠海马内5-HT含量与对照组比较均减少,差异性明显(P<0.05),MT Glu组较Glu组和Luz MT Glu组5-HT含量升高,差异性明显(P<0.05)。结论MT对谷氨酸钠致痫大鼠痫样发作程度、痫样放电有抑制作用,其机制之一是经由其特异性的膜受体,通过某种机制增强5-HT作用,进而发挥抑痫效应。     

高频电刺激对大鼠海马脑片癫痫样放电特性影响的研究

本文采用电极阵列检测技术,在大鼠海马脑切片上诱导出稳定的癫痫样放电,分析、研究130 Hz的高频电刺激(high-frequency stimulation,HFS) CA3区时,海马切片在癫痫发作间期放电(inter-ictal discharges,IID)和发作期放电(ictal discharges,ID)的各项参数、癫痫样放电地起始位点、传播方向和传输速率以及各频段的功率谱密度.结果显示:高频电刺激可以有效地降低癫痫发作期的幅值、减少持续时间、增长潜伏时间、抑制癫痫样放电由IID向ID的转变等.提示高频电刺激抑制癫痫的作用机制是通过促进神经元之间的抑制性传输系统,并且抑制海马神经元之间的兴奋性连接,从而达到抑制效果.     

吗啡诱导大鼠穿梭觅药状态下内侧前额皮层边缘前区遥测脑电小波包提取及熵分析

本研究旨在研究内侧前额皮质(medial prefrontal cortex,m PFC)边缘前区(prelimbic cortical area,PL)遥测脑电的特征性改变与觅药行为之间的关系。将PL区埋藏脑立体定位电极的大鼠分成手术对照组和吗啡诱导组,后者制作吗啡诱导条件性位置偏爱(conditioned place preference,CPP)模型。利用CPP视频系统结合脑电无线遥测技术,记录两组大鼠在黑-白箱穿梭和白-黑箱穿梭时大鼠PL区实时脑电,采用小波包提取、Welch谱功率算法、归一化幅值和Shannon熵分析技术,对所测原始脑电波进行综合分析。结果显示,与手术对照组比较,吗啡诱导CPP组大鼠黑-白箱穿梭潜伏期,左侧PL区小波提取脑电各频段平均波幅减小,脑电成分在10~50 Hz频段Welch谱功率强度显著增加(P0.01或P0.05),脑电β、γ1、γ2波Shannon熵值升高(P0.01或P0.05),平均信息熵降低(P0.01)。上述结果提示,吗啡诱导CPP组大鼠黑-白箱穿梭时,左侧PL区脑电各频段大幅波减少,脑电10~50 Hz频率Welch谱功率强度增加,β、γ1和γ2波Shannon熵值升高;这些变化可能与大鼠觅药意识的形成和即将发动的觅药行为产生有关。     

失血性休克大鼠淋巴管及血管压力对去甲肾上腺素反应的相关性研究

目的:观察失血性休克(HS)大鼠淋巴管与血管对去甲肾上腺素(NE)反应性的变化,探讨淋巴管与血管反应性的关系。方法:大鼠行左侧腹部手术,分离胸导管,测量淋巴管压力(LP);股部手术,经股动脉测量平均动脉血压(MAP)。休克组经股动脉放血复制HS模型(维持MAP40mmHg左右,3h),假手术(sham)组仅手术。在休克不同时间点(或相当),股静脉注射NE(5μg/kg.bw),观察给予NE前后两组大鼠LP以及MAP的变化。结果:休克即刻淋巴管对NE的反应性与sham组无明显差异,到休克0.5h时淋巴管对NE的升压反应开始减弱,至休克3h依然维持低反应性;与sham组相比,休克组血管对NE反应性呈双相表现,休克即刻血管高反应性,休克1h后对NE的升压作用开始减弱,表现为血管低反应性;休克后二者的反应性相关。结论:大鼠HS后淋巴管出现低反应性,且出现在血管低反应性之前;休克发展进程中淋巴管与血管对NE的低反应性呈正相关。     

下坡跑后大鼠腓肠肌成肌调节因子的变化

目的:探讨成肌调节因子(MyoD)在肌肉损伤修复过程中的动态表达,为促进运动肌肉损伤的再生修复提供实验依据。方法:将健康雄性2月龄SD大鼠80只,随机分为对照组(n=10)和下坡运动组(n=70),下坡运动组再分为运动后即刻组、12h、24h、48h、72h、7d和14d组,各运动组动物均进行持续性下坡跑,分别在运动结束后8个时间点麻醉,下腔静脉取血,分离血清,取双侧腓肠肌。常规检测CK、LDH的活性。采用免疫组织化学染色法以及计算机图像分析技术定量统计MyoD因子表达情况。结果:血清CK、LDH在运动后即刻显著上升,后逐渐下降至正常水平。成肌调节因子MyoD在正常骨骼肌中即有表达,各运动组大鼠腓肠肌MyoD因子表达较对照组均有增加,48h组大鼠腓肠肌MyoD免疫阳性细胞核数明显多于对照组(P0.05),后随时间逐渐下降。结论:离心运动后即刻MyoD的表达水平开始上升,48h达到峰值,随后逐渐下降至正常水平。提示成年早期大鼠(2月龄)已具备较成熟的肌肉再生修复能力。     

Retromer Subunits VPS35A and VPS29 Mediate Prevacuolar Compartment （PVC） Function in Arabidopsis

Intracellular protein routing is mediated by vesicular transport which is tightly regulated in eukaryotes. The protein and lipid homeostasis depends on coordinated delivery of de novo synthesized or recycled cargoes to the plasma membrane by exocytosis and their subsequent removal by rerouting them for recycling or degradation. Here, we report the characterization of protein affected trafficking 3 （pat3） mutant that we identified by an epifluorescence-based for- ward genetic screen for mutants defective in subcellular distribution of Arabidopsis auxin transporter PIN1-GFR While pat3 displays largely normal plant morphology and development in nutrient-rich conditions, it shows strong ectopic intracellular accumulations of different plasma membrane cargoes in structures that resemble prevacuolar compart- ments （PVC） with an aberrant morphology. Genetic mapping revealed that pat3 is defective in vacuolar protein sorting 35A （VPS35A）, a putative subunit of the retromer complex that mediates retrograde trafficking between the PVC and trans-Golgi network. Similarly, a mutant defective in another retromer subunit, vps29, shows comparable subcellular defects in PVC morphology and protein accumulation. Thus, our data provide evidence that the retromer components VPS35A and VPS29 are essential for normal PVC morphology and normal trafficking of plasma membrane proteins in plants. In addition, we show that, out of the three VPS35 retromer subunits present in Arabidopsis thaliana genome, the VPS35 homolog A plays a prevailing role in trafficking to the lyric vacuole, presenting another level of complexity in the retromer-dependent vacuolar sorting.     

Role of chaperone-mediated autophagy in degrading Huntington＇s disease-associated huntingtin protein

Mutant N-terminal huntingtin （Htt） protein resulting from Huntington＇s disease （HD） with expanded polyglutamine accumulates and forms aggregates in vulnerable neurons. Both ubiquitin proteasomai and autophagic pathways con- tribute to the degradation of mutant Htt. Here, we focus on the involvement of chaperone-mediated autophagy （CMA）, a selective form of autophagy in the clearance of Htt. Selective catabolism in CMA is conferred by the presence of a KFERQ-Iike targeting motif in the substrates, by which molecular chaperones recognize the hydrophobic surfaces of the misfolded substrates, and transfer them to the lysosomal membrane protein type-2A, LAMP-2A. The substrates are taken into the lysosomes through LAMP-2A and are rapidly degraded by the lysosomal enzymes. Taken together, we summarize the recent evidence to elucidate that Htt is also a potential substrate of CMA. We propose that the manipulation of CMA could be a therapeutic strat- egy for HD.     

Intracellular and Extracellular Phosphatidylinositol 3-Phosphate Produced by Phytophthora Species Is Important for Infection

RxLR effectors produced by Phytophthora pathogens have been proposed to bind to phosphatidylinositol 3-phosphate （Ptdlns（3）P） to mediate their translocation into host cells and/or to increase their stability in planta. Since the levels of Ptdlns（3）P in plants are low, we examined whether Phytophthora species may produce Ptdlns（3）P to pro- mote infection. We observed that Ptdlns（3）P-specific GFP biosensors could bind to P. parasitica and P. sojae hyphae dur- ing infection of Nicotiana benthamiana leaves transiently secreting the biosensors, suggesting that the hyphae exposed Ptdlns（3）P on their plasma membrane and/or secreted Ptdlns（3）R Silencing of the phosphatidylinositol 3-kinases （PI3K） genes, treatment with LY294002, or expression of Ptdlns（3）pobinding proteins by P. sojae reduced the virulence of the pathogen on soybean, indicating that pathogen-synthesized Ptdlns（3）P was required for full virulence. Secretion of Ptdlns（3）P-binding proteins or of a PI3P-5-kinase by N. benthamiana leaves significantly increased the level of resist- ance to infection by P. parasitica and P. capsici. Together, our results support the hypothesis that Phytophthora species produce external Ptdlns（3）P to aid in infection, such as to promote entry of RxLR effectors into host cells. Our results derived from P. sojae RxLR effector Avrlb confirm that both the N-terminus and the C-terminus of this effector can bind Ptdlns（3）P.     

ARMS法检测非小细胞肺癌表皮生长因子受体基因突变及临床意义

目的：探讨应用突变特异性扩增系统法（ARMS）检测非小细胞肺癌（NSCLC）表皮生长因子受体（EGFR）基因突变的特点。方法：收集220例浙江南部地区NSCLC患者肿瘤样本,分别采用ARMS法和测序法检测EGFR基因18、19、20、21号外显子突变情况,并分析EGFR突变与病理类型、突变种类、患者年龄和性别的关系。结果：两方法比较,相符率为86．81％（158/182,Kappa=0．732,P〈0．01）。总突变率为47．27％（104/220）,其中腺癌的突变率明显高于鳞癌（52．46％zJs17．14％;P〈0．01）。肺腺癌中,女性患者EGFR突变率明显高于男性（65．56％∞39．78％;P〈0．01）。突变样本中,21外显子错义突变（L858R）所占比例最高（62．5％,65/104）,19外显子缺失（19Del）其次（43．27％,45/104）,其中两者同时突变占5．77％（6/104）;但腺癌女性与男性患者L858R突变率（64．41％∞56．76％）不存在显著性差别。结论：采用ARMS法检测EGFR基因突变较测序法敏感,突变主要发生在女性肺腺癌患者,以L858R突变为主。     

Prostaglandin E2 modulates F-actin stress fiber in FSS-stimulated MC3T3-E1 cells in a PKA-dependent manner

The effect of prostaglandin E2（PGE2） on bone mass has been well-established in vivo. Previous studies have showed that PGE2 increases differentiation, proliferation, and regu- lates cell morphology through F-actin stress fiber in statically cultured osteoblasts. However, the effect of PGE2 on osteo- blasts in the presence of fluid shear stress （FSS）, which could better uncover the anabolic effect of PGEz in vivo, has yet to be examined. Here, we hypothesized that PGE2 modulates F-actin stress fiber in FSS-stimulated MC3T3-E1 osteoblastic cells through protein kinase A （PKA） pathway. Furthermore, this PGE2-induced F-actin remodeling was associated with the recovery of cellular mechanosensitivity. Our data showed that treatment with 10 nM dmPGE2 for 15 rain significantly suppressed the F-actin stress fiber intensity in FSS-stimulated cells in a PKA-dependent manner. In addition, dmPGE2 treatment enhanced the cells＇ calcium peak magnitude and the percentage of responding cells in the second FSS stimulation, though these effects were abolished and attenuated by co-treatment with phalloidin. Our results demonstrated that 10 nM dmPGE2 was able to accelerate the ＇reset＇ process of F-actin stress fiber to its pre-stimulated level partially through PKA pathway, and thus promoted the recovery of cellular mechanosensitivity. Our finding provided a novel cellular mechanism by which PGE2 increased bone forma- tion as shown in vivo, suggesting that PGE2 could be a potential target for treatments of bone formation-related diseases.     

Thermal comfort and thermoregulation in manned space flight

Exposure to thermal environment is one of the main concerns for manned space exploration. By focusing on the works performed on thermoregulation at microgravity or simulated microgravity, we endeavored to review the investigation on space thermal environmental physiology. First of all, the application of medical requirements for the crew module design from normal thermal comfort to accidental thermal emergencies in a space craft will be addressed. Then, alterations in the autonomic and behavioral temperature regulation caused by the effect of weightlessness both in space flight and its simulation on the ground are also discussed. Furthermore, countermeasures like exercise training, simulated natural ventilation, encouraged drink, etc., in the protection of thermoregulation during space flight is presented. Finally, the challenge of space thermal environment physiology faced in the future is figured out.     

A High-Density SNP Genotyping Array for Rice Biology and Molecular Breeding

A high-density single nucleotide polymorphism （SNP） array is critically important for geneticists and molecu- lar breeders. With the accumulation of huge amounts of genomic re-sequencing data and available technologies for accurate SNP detection, it is possible to design high-density and high-quality rice SNP arrays. Here we report the devel- opment of a high-density rice SNP array and its utility. SNP probes were designed by screening more than 10 000 000 SNP loci extracted from the re-sequencing data of 801 rice varieties and an array named RiceSNP50 was produced on the Illumina Infinium platform. The array contained 51 478 evenly distributed markers, 68% of which were within genic regions. Several hundred rice plants with parent/F1 relationships were used to generate a high-quality cluster file for accurate SNP calling. Application tests showed that this array had high genotyping accuracy, and could be used for dif- ferent objectives. For example, a core collection of elite rice varieties was clustered with fine resolution. Genome-wide association studies （GWAS） analysis correctly identified a characterized QTL. Further, this array was successfully used for variety verification and trait introgression. As an accurate high-throughput genotyping tool, RiceSNP50 will play an important role in both functional genomics studies and molecular breeding.     

Phosphatidic Acid （PA） PP2A Activity and PIN1 Binds PP2AA1 to Regulate Polar Localization

Phospholipase D （PLD） exerts broad biological functions in eukaryotes through regulating downstream effectors by its product, phosphatidic acid （PA）. Protein kinases and phosphatases, such as mammalian target of rapa- mycin （mTOR）, Protein Phosphatase 1 （PP1） and Protein Phosphatase 2C （PP2C）, are PA-binding proteins that execute crucial regulatory functions in both animals and plants. PA participates in many signaling pathways by modulating the enzymatic activity and/or subcellular localization of bound proteins. In this study, we demonstrated that PLD-derived PA interacts with the scaffolding A1 subunit of Protein Phosphatase 2A （PP2A） and regulates PP2A-mediated PIN1 dephos- phorylation in Arabidopsis. Genetic and pharmacological studies showed that both PA and PP2A participate in the regu- lation of auxin distribution. In addition, both the phosphorylation status and polar localization of PIN1 protein were affected by PLD inhibitors, Exogenous PA triggered the membrane accumulation of PP2AA1 and enhanced the PP2A activity at membrane, while PLD inhibition resulted in the reduced endosomal localization and perinuclear aggregation of PP2AA1. These results demonstrate the important role of PLD-derived PA in normal PP2A-mediated PIN dephosphoryl- ation and reveal a novel mechanism, in which PA recruits PP2AA1 to the membrane system and regulates PP2A function on membrane-targeted proteins. As PA and PP2A are conserved among eukaryotes, other organisms might use similar mechanisms to mediate multiple biological processes.