Pub Date : 2003-12-09DOI: 10.4324/9781315542768-11
G. Radvansky
Expression of the rutabaga-encoded type I adenylyl cyclase in Drosophila mushroom bodies can rescue the short-term memory defect in rutabaga mutant flies. In order to differentiate between a potential developmental role of the adenylyl cyclase from its acute function in memory formation, McGuire et al. developed a system to control both temporal and spatial expression of a transgene in Drosophila. Using this system, rutabaga expression in the mushroom bodies during adulthood allowed for normal memory acquisition by otherwise mutant rutabaga animals. This technique will be useful more generally to study when and where gene products are needed during the lifetime of an organism. S. E. McGuire, P. T. Le, A. J. Osborn, K. Matsumoto, R. L. Davis, Spatiotemporal rescue of memory dysfunction in Drosophila. Science 302, 1765-1768 (2003). [Abstract] [Full Text]
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Pub Date : 2003-11-11DOI: 10.1126/scisignal.2082003tw438
There are two Caenorhabditis elegans sexes--male and self-fertilizing hermaphrodite--and males generally represent about 0.1% of a population. Sex is generally determined at fertilization by the ratio of X chromosomes to autosomes. Prahlad et al. now show that sex determination in cross-fertilized C. elegans is plastic and that sexual development can be altered after the embryo stage by exogenous factors. This ability to switch sexual phenotype and karyotype might allow the worm to optimize its development for the environmental conditions encountered. In another example of physiological flexibility, C. elegans can endure adverse environmental conditions by entering into an extreme, but temporary, state of quiescence called suspended animation. Nystul et al. report that for C. elegans to survive through this state in response to severe oxygen deprivation, two components of the mitotic spindle checkpoint pathway are required. In the absence of either of these factors, cells proceeded through metaphase but exhibited chromosomal missegregation. By engaging this mechanism of cell cycle arrest, the organisms ensure genome stability and survival until environmental conditions improve. V. Prahlad, D. Pilgrim, E. B. Goodwin, Roles for mating and environment in C. elegans sex determination. Science 302, 1046-1049 (2003). [Abstract] [Full Text] T. G. Nystul, J. P. Goldmark, P. A. Padilla, M. B. Roth, Suspended animation in C. elegans requires the spindle checkpoint. Science 302, 1038-1041 (2003). [Abstract] [Full Text]
秀丽隐杆线虫有两种性别——雄性和自我受精的雌雄同体——雄性通常占种群总数的0.1%。性别通常在受精时由X染色体与常染色体的比例决定。Prahlad等人现在表明，在交叉受精的秀丽隐杆线虫中，性别决定是可塑的，在胚胎期之后，性发育可以受到外源因素的改变。这种转换性表型和核型的能力可能使蠕虫能够根据所遇到的环境条件优化其发育。在另一个生理灵活性的例子中，秀丽隐杆线虫可以通过进入一种极端但暂时的静止状态来忍受恶劣的环境条件，这种状态被称为假死。Nystul等人报道，秀丽隐杆线虫在严重缺氧状态下存活，需要有丝分裂纺锤体检查点通路的两个组成部分。在没有这些因素的情况下，细胞进入中期，但表现出染色体错分离。通过参与这种细胞周期阻滞机制，生物体确保基因组的稳定性和生存，直到环境条件改善。张建军，张建军，张建军，环境因素对线虫性别决定的影响。科学302,1046-1049(2003)。[摘要][全文]T. G. Nystul, J. P. Goldmark, P. A. Padilla, M. B. Roth，秀丽隐杆线虫的纺锤体检查点对假死的影响。科学学报，2003,38 -1041(2003)。【摘要】【全文】
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Pub Date : 2003-11-11DOI: 10.1126/scisignal.2082003tw436
Heparan sulfate binds to a number of growth factors and morphogens and is highly expressed in the developing mammalian central nervous system (CNS). In order to elucidate heparan sulfate's role in brain development, Inatani et al. selectively knocked out heparan sulfate synthesis in the developing mouse CNS. Mutant mice exhibited malformations in specific regions of the brain that corresponded to disrupted distribution of fibroblast growth factor and decreased cell proliferation. Axon pathfinding in the brain and retina was also disrupted, pointing to additional regulatory functions of heparan sulfate. M. Inatani, F. Irie, A. S. Plump, M. Tessier-Lavigne, Y. Yamaguchi, Mammalian brain morphogenesis and midline axon guidance require heparan sulfate. Science 302, 1044-1046 (2003). [Abstract] [Full Text]
{"title":"Heparan Sulfate in Brain Development","authors":"","doi":"10.1126/scisignal.2082003tw436","DOIUrl":"https://doi.org/10.1126/scisignal.2082003tw436","url":null,"abstract":"Heparan sulfate binds to a number of growth factors and morphogens and is highly expressed in the developing mammalian central nervous system (CNS). In order to elucidate heparan sulfate's role in brain development, Inatani et al. selectively knocked out heparan sulfate synthesis in the developing mouse CNS. Mutant mice exhibited malformations in specific regions of the brain that corresponded to disrupted distribution of fibroblast growth factor and decreased cell proliferation. Axon pathfinding in the brain and retina was also disrupted, pointing to additional regulatory functions of heparan sulfate. M. Inatani, F. Irie, A. S. Plump, M. Tessier-Lavigne, Y. Yamaguchi, Mammalian brain morphogenesis and midline axon guidance require heparan sulfate. Science 302, 1044-1046 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"50 1","pages":"tw436 - tw436"},"PeriodicalIF":0.0,"publicationDate":"2003-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76064246","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-10-28DOI: 10.1126/scisignal.2062003tw419
E. J. Debeljak
Rajasekhar et al. used gene expression profiling to compare the effect of oncogenic Ras and Akt signaling on total cellular mRNA and polysomal mRNA and discovered that the immediate effects of signaling through these two pathways on recruitment of specific existing mRNAs to polysomes were far greater than on transcription. Glioblastoma, a highly malignant form of brain cancer, is frequently characterized by increased activity of Ras and Akt; moreover, combined activation of Ras and Akt signaling pathways in glial progenitor cells promotes glioblastoma formation. Rajasekhar used mouse glial progenitor cells expressing constitutively active K-Ras, constitutively active Akt, or both, in combination with small molecule inhibitors of these signaling pathways, to investigate their effects on translational efficiency. Microarray analysis of total cellular mRNA indicated that, of 12,488 genes screened, fewer than 20 genes showed a greater than threefold change in mRNA levels after 2 hours' blockade of Akt or Ras signaling. In contrast, a screen of mRNA associated with polysomes (purified with sucrose gradients) revealed a decrease in the polysome association of hundreds of mRNAs by a factor greater than 3 in response to Akt or Ras blockade, with levels of many changing by a factor greater than 10. Among mRNAs identified as showing changes in polysome association in response to both activation of Ras and Akt signaling and pharmacological inhibition of either pathway were many implicated in oncogenic signaling pathways, as well as many known transcription factors. Thus, the authors propose that the oncogenic effects of Ras and Akt signaling may initially arise predominantly from changes in mRNA translation. V. K. Rajasekhar, A. Viale, N. D. Socci, M. Wiedmann, X. Hu, E. C. Holland, Oncogenic Ras and Akt signaling contribute to glioblastoma formation by differential recruitment of existing mRNAs to polysomes. Mol. Cell 12, 889-901 (2003). [Online Journal]
Rajasekhar等人利用基因表达谱比较了致癌Ras和Akt信号传导对细胞总mRNA和多体mRNA的影响，发现通过这两种途径的信号传导对现有特异性mRNA向多体募集的直接影响远大于对转录的影响。胶质母细胞瘤是一种高度恶性的脑癌，通常以Ras和Akt活性增加为特征;此外，神经胶质祖细胞中Ras和Akt信号通路的联合激活促进了胶质母细胞瘤的形成。Rajasekhar使用表达组成性活性K-Ras或组成性活性Akt或两者的小鼠胶质祖细胞，结合这些信号通路的小分子抑制剂，研究它们对翻译效率的影响。细胞总mRNA的微阵列分析表明，在筛选的12488个基因中，只有不到20个基因在阻断Akt或Ras信号2小时后mRNA水平发生了3倍以上的变化。相比之下，与多聚体相关的mRNA(用蔗糖梯度纯化)的筛选显示，在Akt或Ras阻断的作用下，数百种mRNA的多聚体关联减少了3倍以上，许多mRNA的水平变化了10倍以上。在Ras和Akt信号的激活和任何一种途径的药理抑制反应中显示多体关联变化的mrna中，许多与致癌信号通路以及许多已知的转录因子有关。因此，作者提出Ras和Akt信号的致癌作用最初可能主要来自mRNA翻译的变化。V. K. Rajasekhar, A. Viale, N. D. Socci, M. Wiedmann, X. Hu, E. C. Holland，肿瘤基因Ras和Akt信号在胶质母细胞瘤形成中的作用。分子细胞12,889-901(2003)。(在线期刊)
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Pub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw409
G. Chin
A conformational change in the prion protein (PrPC) results in the production of a neurotoxic form, PrPSc, which is implicated in transmissible spongiform encephalopathies. Hetz et al. determined that application of PrPSc to N2A neuroblastoma cells triggered apoptosis and activation of caspase-3, but not caspase-8 or caspase-1. PrPSc stimulated an increase in intracellular calcium concentration [Ca2+]i, resulting from release from the endoplasmic reticulum (ER)--increased [Ca2+]i was observed in the absence of extracellular calcium and was diminished by treatment of the cells with the ER calcium pump inhibitor thapsigargin. Application of PrPSc stimulated activation of the ER resident caspase-12 and increased expression of the ER chaperones, Grp94, Grp78, and Grp58, indicating that PrPSc triggered the ER stress response. The toxic effects of PrPSc or other triggers of ER stress were decreased in cells expressing a dominant-negative caspase-12 mutant. Although infection of N2A cells with prion protein (to endogenously express the PrPSc instead of exogenously applying the toxic protein) did not cause decreased cell viability under resting conditions, the infected cells were more sensitive to triggers of ER stress and showed decreased viability compared with uninfected cells. In mice infected with prion (139A-scrapie), active caspase-12 was detectable in the brain and regions of the brain with the highest caspase-12 activity also showed the most neuronal death. In addition, the brains of infected mice showed an increase in a subset of ER chaperones. Postmortem analysis of brain tissue from patients with Creutzfeldt-Jakob disease showed increased ER chaperones and active caspase-12, along with protease-resistant PrPSc. Thus, the ER stress response may play a critical role in the toxicity of prions, and the results suggest that this pathway may be a target for pharmacological intervention. C. Hetz, M. Russelakis-Carneiro, K. Maundrell, J. Castilla, C. Soto, Caspase-12 and endoplasmic reticulum stress mediate neurotoxicity of pathological prion protein. EMBO J.22, 5435-5445 (2003). [Abstract] [Full Text]
朊病毒蛋白(PrPC)的构象变化导致神经毒性PrPSc的产生，这与传染性海绵状脑病有关。Hetz等人发现，将PrPSc应用于N2A神经母细胞瘤细胞会触发凋亡和caspase-3的激活，但不会触发caspase-8或caspase-1。PrPSc刺激了细胞内钙浓度[Ca2+]i的增加，这是由内质网(ER)的释放引起的——在缺乏细胞外钙的情况下观察到[Ca2+]i的增加，并通过内质网钙泵抑制剂thapsigarin处理细胞而减少。应用PrPSc刺激内质网驻留caspase-12的激活，并增加内质网伴侣Grp94、Grp78和Grp58的表达，表明PrPSc触发内质网应激反应。在表达显性阴性caspase-12突变体的细胞中，PrPSc或其他内质网应激触发器的毒性作用降低。虽然用朊病毒蛋白感染N2A细胞(内源性表达PrPSc而不是外源性应用有毒蛋白)在静息条件下不会导致细胞活力下降，但与未感染细胞相比，感染细胞对内质网应激的触发更敏感，并且表现出活力下降。在感染了朊病毒(139A-scrapie)的小鼠中，可以在大脑中检测到活性的caspase-12, caspase-12活性最高的大脑区域也显示出最多的神经元死亡。此外，受感染小鼠的大脑显示出ER伴侣亚群的增加。克雅氏病患者的脑组织尸检分析显示，ER伴侣和活性caspase-12增加，同时伴有蛋白酶抗性PrPSc。因此，内质网应激反应可能在朊病毒毒性中起关键作用，结果表明该途径可能是药物干预的靶点。C. Hetz, M. Russelakis-Carneiro, K. Maundrell, J. Castilla, C. Soto, Caspase-12和内质网应激介导病理性朊蛋白的神经毒性。[j] .中国生物医学工程学报，2003,22(5):535 - 545。【摘要】【全文】
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Pub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw416
Semiconductor quantum dots (QDs) have recently emerged as probes with the potential to revolutionize fluorescence imaging. Dahan et al. have now detected single QD-tagged glycine receptors in living cultured spinal neurons. By combining in vivo monitoring and post hoc electron microscopic analysis, the dynamics of receptors was monitored over time and the entry of a receptor into the synapse was directly observed. M. Dahan, S. Lévi, C. Luccardini, P. Rostaing, B. Riveau, A. Triller, Diffusion dynamics of glycine receptors revealed by single-quantum dot tracking. Science 302, 442-445 (2003). [Abstract] [Full Text]
半导体量子点(QDs)最近作为探针出现，具有彻底改变荧光成像的潜力。Dahan等人现在已经在活培养的脊髓神经元中检测到单个qd标记的甘氨酸受体。通过结合体内监测和事后电镜分析，随着时间的推移监测受体的动态，并直接观察受体进入突触的情况。M. Dahan, S. l vi, C. Luccardini, P. Rostaing, B. Riveau, A. Triller，单量子点跟踪研究甘氨酸受体的扩散动力学。科学302,442-445(2003)。【摘要】【全文】
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Pub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw415
D. Rakosy
In most plant-pollinator relationships, the plant is cross-fertilized while the pollinator gains a food reward. In sexually deceptive orchids, the flower mimics a female insect in shape, color, and odor, and males are deceived into "mating" with the flowers, thus transferring pollen without receiving a reward. Schiestl et al. describe an extreme example of this phenomenon in an Australian orchid. The flower produces a volatile compound, 2-ethyl-5-propylcyclohexan-1,3-dione, that is identical in all respects to a pheromone produced by females of its pollinating thynnine wasp. Such dependence on a single compound is highly unusual and may imply limited evolutionary flexibility; nevertheless, the occurrence of more than 300 thynnine-orchid pollination relationships suggests that other highly specific communication systems may occur in nature. F. P. Schiestl, R. Peakall, J. G. Mant, F. Ibarra, C. Schulz, S. Franke, W. Francke, The chemistry of sexual deception in an orchid-wasp pollination system. Science 302, 437-438 (2003). [Abstract] [Full Text]
在大多数植物与传粉者的关系中，植物进行交叉受精，而传粉者获得食物奖励。在有性欺骗的兰花中，花在形状、颜色和气味上模仿雌性昆虫，雄性昆虫被欺骗与花“交配”，从而在没有得到奖励的情况下传递花粉。Schiestl等人在一种澳大利亚兰花上描述了这种现象的一个极端例子。这种花产生一种挥发性化合物，2-乙基-5-丙基环己烷-1,3-二酮，在所有方面都与雌性传粉的九蜂产生的信息素相同。这种对单一化合物的依赖是非常不寻常的，可能意味着有限的进化灵活性;然而，超过300种九兰传粉关系的出现表明，自然界中可能存在其他高度特异性的交流系统。F. P. Schiestl, R. Peakall, J. G. Mant, F. Ibarra, C. Schulz, S. Franke, W. Francke，兰花-黄蜂传粉系统中性欺骗的化学反应。科学302,437-438(2003)。【摘要】【全文】
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Pub Date : 2003-10-14DOI: 10.1126/scisignal.2042003tw406
Neuronal axons form branches to establish precise connections with their targets, but branch control is not well understood. Colavita and Tessier-Lavigne have identified a subset of neurons in Caenorhabditis elegans that require a membrane protein called BAM-2 (branching abnormal) to stop formation of branches and to stabilize their termination. Loss of BAM-2 allowed branches to overshoot their normal termination sites. BAM-2 shows sequence similarity to neurexins that are thought to control the stability of neuronal synapses. A. Colavita, M. Tessier-Lavigne, A neurexin-related protein, BAM-2, terminates axonal branches in C. elegans. Science 302, 293 (2003). [Abstract] [Full Text]
神经元轴突形成分支以与它们的目标建立精确的连接，但分支控制尚不清楚。Colavita和Tessier-Lavigne已经在秀丽隐杆线虫中发现了一个神经元子集，它需要一种叫做BAM-2(分支异常)的膜蛋白来阻止分支的形成并稳定它们的终止。bam2的缺失使得分支超过了它们正常的终止位点。bam2的序列与被认为控制神经元突触稳定性的神经素相似。A. Colavita, M. Tessier-Lavigne，神经素相关蛋白bam2在线虫轴突分支终止中的作用。科学302,293(2003)。【摘要】【全文】
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Pub Date : 2003-09-30DOI: 10.1126/scisignal.2022003tw377
Many proteins behave like complex switches, integrating multiple inputs to control downstream outputs. It has been thought that such switches could evolve through recombination of their modular domains. Dueber et al. demonstrate this principle by showing that the actin-polymerizing activity of neuronal Wiskott-Aldrich syndrome protein (WASP) can be reprogrammed to respond to unnatural input by replacing input domains with heterologous ones. Achieving switch diversity through this process could underlie the evolution of signaling circuits. J. E. Dueber, B. J. Yeh, K. Chak, W. A. Lim, Reprogramming control of an allosteric signaling switch through modular recombination. Science 301, 1904-1908 (2003). [Abstract] [Full Text]
{"title":"Modular Switches","authors":"","doi":"10.1126/scisignal.2022003tw377","DOIUrl":"https://doi.org/10.1126/scisignal.2022003tw377","url":null,"abstract":"Many proteins behave like complex switches, integrating multiple inputs to control downstream outputs. It has been thought that such switches could evolve through recombination of their modular domains. Dueber et al. demonstrate this principle by showing that the actin-polymerizing activity of neuronal Wiskott-Aldrich syndrome protein (WASP) can be reprogrammed to respond to unnatural input by replacing input domains with heterologous ones. Achieving switch diversity through this process could underlie the evolution of signaling circuits. J. E. Dueber, B. J. Yeh, K. Chak, W. A. Lim, Reprogramming control of an allosteric signaling switch through modular recombination. Science 301, 1904-1908 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"39 1","pages":"TW377 - tw377"},"PeriodicalIF":0.0,"publicationDate":"2003-09-30","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"87517618","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
Pub Date : 2003-09-23DOI: 10.1126/scisignal.2012003tw369
Association of the T cell coreceptors CD-4 and CD-8 with the cytoplasmic kinase Lck regulates T cell activation and maturation. Kim et al. have explored the requirement for zinc in this interaction and report that the metal ion acts as a clasp that stabilizes a receptor-Lck complex. Peptides corresponding to a short region of Lck and in either receptor's cytoplasmic tail were unordered, but the presence of zinc induced the synergistic mutual folding of the peptides. Protein modifications could unlatch the clasp and modulate receptor-Lck binding. P. W. Kim, Z.-Y. J. Sun, S. C. Blacklow, G. Wagner, M. J. Eck, A zinc clasp structure tethers Lck to T cell coreceptors CD4 and CD8. Science 301, 1725-1728 (2003). [Abstract] [Full Text]
{"title":"Zinc Links in a Receptor-Kinase Complex","authors":"","doi":"10.1126/scisignal.2012003tw369","DOIUrl":"https://doi.org/10.1126/scisignal.2012003tw369","url":null,"abstract":"Association of the T cell coreceptors CD-4 and CD-8 with the cytoplasmic kinase Lck regulates T cell activation and maturation. Kim et al. have explored the requirement for zinc in this interaction and report that the metal ion acts as a clasp that stabilizes a receptor-Lck complex. Peptides corresponding to a short region of Lck and in either receptor's cytoplasmic tail were unordered, but the presence of zinc induced the synergistic mutual folding of the peptides. Protein modifications could unlatch the clasp and modulate receptor-Lck binding. P. W. Kim, Z.-Y. J. Sun, S. C. Blacklow, G. Wagner, M. J. Eck, A zinc clasp structure tethers Lck to T cell coreceptors CD4 and CD8. Science 301, 1725-1728 (2003). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"5 1","pages":"TW369 - tw369"},"PeriodicalIF":0.0,"publicationDate":"2003-09-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83776472","PeriodicalName":null,"FirstCategoryId":null,"ListUrlMain":null,"RegionNum":0,"RegionCategory":"","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":"","EPubDate":null,"PubModel":null,"JCR":null,"JCRName":null,"Score":null,"Total":0}
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