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A Highway for War and Peace： The Secretory Pathway in Plant-Microbe Interactions

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Molecular Plant 2011年第4期4卷 581-587页

作者： Dong Wang Xinnian Dong Department of Biology Stanford University Stanford CA 94305 USA Department of Biology PO Box 90338 Duke University Durham NC 27707 USA

Secretion of proteins and other molecules is the primary means by which a cell interacts with its surroundings. The overall organization of the secretory system is remarkably conserved among eukaryotes, and many of the components have been investigated in detail in animal models. Plant cells, because of their sessile lifestyle, are uniquely reliant on the secretory pathway to respond to changes in their environments, either abiotic, such as the absence of nutrients, or biotic, such as the presence of predators or pathogens. In particular, most plant pathogens are extracellular, which demands a robust and efficient host secretory system directed at the site of attack. Here, we present a summary of recent advances in our understanding of the molecular details of the secretory pathway during plant-microbe interactions. Secretion is required not only for the delivery of antimicrobial molecules, but also for the biogenesis of cell surface sensors to detect microbes. The deposition of extracellular material is important in the defense against classical bacterial pathogens as well as in the so-called ＂non-host＇ resistance. Finally, boosting the protein secretion capacity is vital for avoiding infection as well as for achieving symbiosis, even though in the latter case, the microbes are engulfed in intracellular compartments. The emerging evidence indicates that secretion provides an essential interface between plant hosts and their associated microbial partners.

关键词： protein secretion defense salicylic acid NPR1 symbiosis Arabidopsis legume endoplasmic reticulum SNARE.

蛋白质O-GlcNAc糖基化修饰对tau蛋白磷酸化修饰的影响

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生物化学与生物物理进展 2003年第4期30卷 623-628页

作者：钱慰刘飞朱俐龚成新金淑仪南通医学院生物化学教研室南通226001 Department of Neurochemistry NYS Institute for Basic Research in Developmental Disabilities New York 10314USA 南通医学院生物化学教研室南通226001Department of Neurochemistry NYS Institute for Basic Research in Developmental Disabilities New York 10314USA

蛋白质的O位N 乙酰葡萄糖胺 (O GlcNAc)糖基化修饰是一种新近发现的广泛存在于细胞核蛋白与细胞浆蛋白的蛋白质翻译后修饰 .其性质与经典的膜蛋白和分泌蛋白的糖基化修饰不同 ,而与蛋白质磷酸化修饰更相似 .O GlcNAc糖基化和磷酸化均修... 详细信息

蛋白质的O位N 乙酰葡萄糖胺 (O GlcNAc)糖基化修饰是一种新近发现的广泛存在于细胞核蛋白与细胞浆蛋白的蛋白质翻译后修饰 .其性质与经典的膜蛋白和分泌蛋白的糖基化修饰不同 ,而与蛋白质磷酸化修饰更相似 .O GlcNAc糖基化和磷酸化均修饰tau蛋白的丝氨酸和苏氨酸残基 ,通过改变O GlcNAc糖基化供体底物浓度以及其关键酶活性等方法 ,改变分化后成神经细胞样的PC12细胞中的蛋白质O GlcNAc糖基化修饰水平 ,然后用特异性识别不同位点磷酸化的tau蛋白抗体 ,进行蛋白质印迹分析来检测tau蛋白磷酸化水平的变化 .结果发现细胞内蛋白质O GlcNAc糖基化对tau蛋白磷酸化的影响 ,在不同的磷酸化位点其影响不同 .增加蛋白质O GlcNAc糖基化修饰导致tau蛋白大多数磷酸位点的磷酸化水平降低 ,反之亦然 .这些结果说明 ,tau磷酸化在大多数位点受到O GlcNAc糖基化修饰的负性调节 .

关键词：蛋白质糖基化修饰 tau蛋白磷酸化修饰

小鼠局灶性脑缺血后ICAM-1、Mac-1和MPO活性的变化

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复旦学报（医学版） 2003年第4期30卷 304-307,F002页

作者：王知秋陈衔城杨国源周良辅复旦大学附属华山医院神经病学研究所神经外科上海200040 美国加里弗尼亚州立大学总医院脑血管研究中心旧金山94110

目的研究缺血脑组织内的炎症反应过程及其在缺血基底节及其周围皮质的不同特征。方法用线栓法制作小鼠大脑中动脉持续性栓塞模型(pMCAO),用免疫组化法观察缺血区血管内皮细胞黏附因子ICAM-1和白细胞Mac-1的表达,测定髓过氧化物酶(MPO... 详细信息

目的研究缺血脑组织内的炎症反应过程及其在缺血基底节及其周围皮质的不同特征。方法用线栓法制作小鼠大脑中动脉持续性栓塞模型(pMCAO),用免疫组化法观察缺血区血管内皮细胞黏附因子ICAM-1和白细胞Mac-1的表达,测定髓过氧化物酶(MPO)活性。结果 MCAO后4 h,缺血区ICAM-1阳性血管开始增加,24～48 h达高峰,72 h后减少;各时段缺血皮质区的阳性血管数均多于基底节。MCAO后24 h缺血基底节Mac-1阳性细胞明显增加,48 h到达顶峰,72 h后缓慢减少;而在缺血皮质,MCAO后4 h,Mac-1阳性白细胞已开始增加,48 h达到顶峰,72 h后仍保持较高的数量,各时段缺血皮质区的Mac-1阳性细胞数均多于基底节区。MCAO后12 h缺血基底节MPO活性开始升高,24 h到达高峰,72 h后逐步下降;在缺血皮质,MCAO后12 hMPO活性小幅升高,24 h后达到顶峰,并维持较高水平至120 h。结论小鼠大脑中动脉持续性栓塞早期,缺血脑组织ICAM-1、Mac-1表达和MPO活性平行升高,提示小鼠局灶性脑缺血后存在缺血性损伤诱导的主动性炎症反应,与缺血基底节区相比,周围皮质的炎症反应更为持久而强烈。

关键词：局灶性脑缺血 ICAM-1 Mac-1 MPO 免疫组化法线栓法小鼠

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细胞外信号调节激酶在局灶性脑缺血中的作用

复旦学报（医学版） 2003年第6期30卷 527-530页

作者：王知秋陈衔城周良辅吴笃初车晓明杨国源复旦大学附属华山医院神经病学研究所神经外科上海200040 美国密歇根大学神经外科克洛司比研究室密歇根州48109

目的研究细胞外信号调节激酶(ERK)在局灶性脑缺血中的作用。方法线栓法制作小鼠大脑中动脉栓塞(MCAO)模型。通过Western blot和免疫组织化学方法研究磷酸化ERK1/2的活性特征。静脉内应用ERK通路阻滞剂U0126,测定缺血小鼠的神经系统损... 详细信息

目的研究细胞外信号调节激酶(ERK)在局灶性脑缺血中的作用。方法线栓法制作小鼠大脑中动脉栓塞(MCAO)模型。通过Western blot和免疫组织化学方法研究磷酸化ERK1/2的活性特征。静脉内应用ERK通路阻滞剂U0126,测定缺血小鼠的神经系统损害和脑梗死体积的改变。结果 MCAO后30min,磷酸化ERK1/2在局灶缺血小鼠脑组织中显著升高,2h达到最高峰,6h恢复。免疫组化研究显示磷酸化ERK1/2阳性细胞在梗死基底节和周围皮质大量出现。荧光双染提示磷酸化ERK1/2阳性的细胞为神经元和星形细胞。与对照组相比,注射U0126的脑缺血小鼠神经损伤评分降低44.6％,梗死体积降低54.4％。结论 ERK在小鼠局灶性脑缺血中起着重要的作用,阻断ERK通路对缺血性脑损伤有一定保护作用,并可能成为脑缺血治疗的新途径。

关键词：细胞外信号调节激酶局灶性脑缺血大脑中动脉栓塞神经系统损害小鼠

Early Growth Response gene 1 (Egr-1) regulates HSV-1 ICP4 and ICP22 gene expression

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Cell Research 2007年第6期17卷 546-555页

作者： Gautam R Bedadala Rajeswara C Pinnoji Shao-Chung V Hsia Department of Basic Pharmaceutical Sciences College of Pharmacy The University of Louisiana at Monroe 700 University AvenueMonroeLA 71209 USA

The molecular mechanisms mediating herpes simplex virus type 1 (HSV-1) gene silencing during latent infection arenot clear. Five copies of early growth response gene 1 (Egr-1) binding elements were identified in the intron of HSV-1ICP22 (infected cell protein No. 22) gene, leading to the hypothesis that Egr-1 binds to the viral genome and regulates theviral gene expression. Transient co-transfection assays indicated that Egr-1 negatively regulated the transcription of bothfull-length and intron-removed ICP22 promoters. The same assays also revealed that Egr-1 repressed ICP4 (infected cellprotein No. 4) promoter activity in a dose-dependent manner but showed less inhibition when the intron was *** deacetylation was not involved in this regulation since histone deacetylase inhibitor trichostatin Adid not exhibitany effect on Egr-1-mediated repression. Chromatin immunoprecipitation assays showed that Egr-1 reduced the bindingof Spl to the promoters and that the co-repressor Nab2 (NGFI-A/EGR1-binding protein) was recruited to the proximityof ICP4 in the presence of Egr-1. These results suggested that the multifunctional transcription factor Egr-1 can repressHSV-1 immediate-early gene expression through the recruitment of co-repressor Nab2 and reduction of Sp1 occupancy,and thus may play a critical role in HSV-1 gene silencing during latency.

关键词： HSV-1 latency Egr-1 Sp1 Nab2 transcription regulation

An Autophosphorylation Site of the Protein Kinase SOS2 Is Important for Salt Tolerance in Arabidopsis

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Molecular Plant 2009年第1期2卷 183-190页

作者： Hiroaki Fujii Jian-Kang Zhu Department of Botany and Plant Sciences 2150 Batchelor Hall University of California Riverside CA 92521 USA

The protein kinase SOS2 （Salt Overly Sensitive 2） is essential for salt-stress signaling and tolerance in Arabidopsis. SOS2 is known to be activated by calcium-SOS3 and by phosphorylation at its activation loop. SOS2 is autophosphorylated in vitro, but the autophosphorylation site and its role in salt tolerance are not known. In this study, we identified an autophosphorylation site in SOS2 and analyzed its role in the responses of Arabidopsis to salt stress. Mass spectrometry analysis showed that Ser 228 of SOS2 is autophosphorylated. When this site was mutated to Ala, the autophosphorylation rate of SOS2 decreased. The substrate phosphorylation by the mutated SOS2 was also less than that by the wild-type SOS2. In contrast, changing Ser228 to Asp to mimic the autophosphorylation enhanced substrate phosphorylation by SOS2. Complementation tests in a sos2 mutant showed that the S228A but not the $228D mutation partially disrupted the function of SOS2 in salt tolerance. We also show that activation loop phosphorylation at Thr168 and autophosphorylation at Ser228 cannot substitute for each other, suggesting that both are required for salt tolerance. Our results indicate that Ser 228 of SOS2 is autophosphorylated and that this autophosphorylation is important for SOS2 function under salt stress.

关键词： SOS2 autophosphorylation salt tolerance protein kinase Arabidopsis

A Light-Independent Allele of Phytochrome B Faithfully Recapitulates Photomorphogenic Transcriptional Networks

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Molecular Plant 2009年第1期2卷 166-182页

作者： Wei Hu Yi-Shin Su J. Clark Lagarias Department of Molecular and Cellular Biology College of Biological Sciences University of California Davis CA 95616 USA Present address: Carnegie Institution of Washington -Department of Plant Biology Stanford CA 94305 USA

Dominant gain-of-function alleles of Arabidopsis phytochrome B were recently shown to confer lightindependent, constitutive photomorphogenic （cop） phenotypes to transgenic plants （Su and Lagarias, 2007）. In the present study, comparative transcription profiling experiments were performed to assess whether the pattern of gene expression regulated by these alleles accurately reflects the process of photomorphogenesis in wild-type Arabidopsis. Whole- genome transcription profiles of dark-grown phyAphyB seedlings expressing the Y^276H mutant of phyB （YHB） revealed that YHB reprograms about 13% of the Arabidopsis transcriptome in a light-independent manner. The YHB-regulated transcriptome proved qualitatively similar to but quantitatively greater than those of wild-type seedlings grown under 15 or 50 μmol m^-2 m^-1 continuous red light （Rc）. Among the 2977 genes statistically significant two-fold （SSTF） regulated by YHB in the absence of light include those encoding components of the photosynthetic apparatus, tetrapyrrole/pigment biosynthetic pathways, and early light-responsive signaling factors. Approximately 80% of genes SSTF regulated by Rc were also YHB-regulated. Expression of a notable subset of 346 YHB-regulated genes proved to be strongly attenuated by Rc, indicating compensating regulation by phyC-E and/or other Rc-dependent processes. Since the majority of these 346 genes are regulated by the circadian clock, these results suggest that phyA- and phyB-independent light signaling pathway（s） strongly influence clock output. Together with the unique plastid morphology of dark-grown YHB seedlings, these analyses indicate that the YHB mutant induces constitutive photomorphogenesis via faithful reconstruction of phyB signaling pathways in a light-independent fashion.

关键词： light signaling signal transduction transcriptome analysis photomorphogenesis Arabidopsis phytochrome.

Microchimerism in recurrent miscarriage

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Cellular & Molecular Immunology 2014年第6期11卷 589-594页

作者： Hilary S Gammill Mary D Stephenson Tessa M Aydelotte J Lee Nelson Clinical Research Division Fred Hutchinson Cancer Research Center Seattle WA USA Department of Obstetrics & Gynecology University of Washington Seattle WA USA Department of Obstetrics and Gynecology University of Chicago Chicago IL USA and Department of Obstetrics and Gynecology University of Illinois at Chicago Chicago IL USA Division of Rheumatolegy University of Washington Seattle WA USA

Maternal-fetal cell exchange during pregnancy results in acquisition of microchimerism, which can durably persist in both recipients. Naturally acquired microchimerism may impact maternal-fetal interaction in pregnancy. We conducted studies to ask whether microchimerism that a woman acquired from her own mother is detectable before or during pregnancy in women with recurrent miscarriage. Fetal microchimerism was also assayed. Women with primary idiopathic recurrent miscarriage （n=23） and controls （n=31） were studied. Genotyping was conducted for probands, their mothers and the fetus, a non-shared polymorphism identified and quantitative polymerase chain reaction performed to measure microchimerismin peripheral blood mononuclear cells. Preconception comparisons were made between recurrent miscarriage subjects and controls, using logistic regression and Wilcoxon rank sum. Longitudinal microchimerism in subsequent pregnancies of recurrent miscarriage subjects was described. There was a trend toward lower preconception detection of microchimerism in recurrent miscarriage versus controls, 6% vs. 19% （1/16 vs. 6/31, P=0.2）. During pregnancy, 3111 （27%） of recurrent miscarriage subjects who went on to have a birth had detection of microchimerism from their own mother, whereas neither of two subjects who went on to miscarry had detection （0/2）. This initial data suggest that microchimerism from a woman＇s own mother, while detectable in women with recurrent miscarriage, may differ from controls and according to subsequent pregnancy outcome. Further studies are needed to determine the cell types,quantities and any potential functional role of microchimerism in recurrent miscarriage.

关键词： microchimerism pregnancy recurrent miscarriage reproduction

Protein phosphatase PP1γ2 in sperm morphogenesis and epididymal initiation of sperm motility

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Asian Journal of Andrology 2007年第4期9卷 445-452页

作者： Rumela Chakrabarti Lina Cheng Pawan Purl David Soler Srinivasan Vijayaraghavan Department of Biological Sciences Kent State University Kent OH 44242-0001 USA

The serine/threonine phosphatase （PP1） isoform PP1γ2, predominantly expressed in the testis, is a key enzyme in spermatozoa. High PP1γ2 catalytic activity holds motility in check in immature spermatozoa. Inhibition of PP1γ2 causes motility initiation in immature spermatozoa and motility stimulation and changes in flagellar beat parameters in mature spermatozoa. The PP1γ2 isoform is present in all mammalian spermatozoa studied： mouse, rat, hamster, bovine, non-human primate and man. We have now identified at least four of its regulatory proteins that regulate distinct pools of PP1γ2 within spermatozoa. Our studies provide new insights into biochemical mechanisms underlying development and regulation of sperm motility. We hypothesize that changes in sperm PP1γ2 activity as a result of phosphorylation and reversible binding of the regulatory proteins to the catalytic subunit are critical in the development and regulation of motility and the ability of sperm to fertilize eggs. Targeted disruption of the Ppplcc gene, which encodes the PP1γ1 or PP1γ2 isoforms, causes male infertility in mice as a result of impaired spermiogenesis. Our observations suggest that, in addition to motility, the protein phosphatase PP1γ2 might play an isoform-specific function in the development of specialized flagellar structures of mammalian spermatozoa. （Asian J Androl 2007 July; 9： 445--452）

关键词： protein phosphatase epididymis sperm motility spermatogenesis