Science's STKEPub Date : 2003-12-09DOI: 10.4324/9781315542768-11
G. Radvansky
{"title":"Memory in Space and Time","authors":"G. Radvansky","doi":"10.4324/9781315542768-11","DOIUrl":"https://doi.org/10.4324/9781315542768-11","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"49 1","pages":"TW475 - tw475"},"PeriodicalIF":0.0,"publicationDate":"2003-12-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75121604","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}
Science's STKEPub Date : 2003-11-11DOI: 10.1126/scisignal.2082003tw438
{"title":"Flexible Sex and Suspended Animation in Nematodes","authors":"","doi":"10.1126/scisignal.2082003tw438","DOIUrl":"https://doi.org/10.1126/scisignal.2082003tw438","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"65 1","pages":"tw438 - tw438"},"PeriodicalIF":0.0,"publicationDate":"2003-11-11","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"83377298","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}
Science's STKEPub Date : 2003-11-11DOI: 10.1126/scisignal.2082003tw436
{"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}
Science's STKEPub Date : 2003-10-28DOI: 10.1126/scisignal.2062003tw419
E. J. Debeljak
{"title":"Gained in Translation?","authors":"E. J. Debeljak","doi":"10.1126/scisignal.2062003tw419","DOIUrl":"https://doi.org/10.1126/scisignal.2062003tw419","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"7 1","pages":"tw419 - tw419"},"PeriodicalIF":0.0,"publicationDate":"2003-10-28","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82373951","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}
Science's STKEPub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw409
G. Chin
{"title":"Prions Stress Out the ER","authors":"G. Chin","doi":"10.1126/scisignal.2052003tw409","DOIUrl":"https://doi.org/10.1126/scisignal.2052003tw409","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"43 1","pages":"TW409 - tw409"},"PeriodicalIF":0.0,"publicationDate":"2003-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73580161","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}
Science's STKEPub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw416
{"title":"Glycine Receptors On the Move","authors":"","doi":"10.1126/scisignal.2052003tw416","DOIUrl":"https://doi.org/10.1126/scisignal.2052003tw416","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"17 1","pages":"TW416 - tw416"},"PeriodicalIF":0.0,"publicationDate":"2003-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"89244448","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}
Science's STKEPub Date : 2003-10-21DOI: 10.1126/scisignal.2052003tw415
D. Rakosy
{"title":"Sexual Deception by Orchids","authors":"D. Rakosy","doi":"10.1126/scisignal.2052003tw415","DOIUrl":"https://doi.org/10.1126/scisignal.2052003tw415","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"2003 1","pages":"TW415 - tw415"},"PeriodicalIF":0.0,"publicationDate":"2003-10-21","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75372788","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}
Science's STKEPub Date : 2003-10-14DOI: 10.1126/scisignal.2042003tw406
{"title":"Knowing When to Branch","authors":"","doi":"10.1126/scisignal.2042003tw406","DOIUrl":"https://doi.org/10.1126/scisignal.2042003tw406","url":null,"abstract":"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]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"2015 1","pages":"TW406 - tw406"},"PeriodicalIF":0.0,"publicationDate":"2003-10-14","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86256016","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}
Science's STKEPub Date : 2003-09-30DOI: 10.1126/scisignal.2022003tw377
{"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}
Science's STKEPub Date : 2003-09-23DOI: 10.1126/scisignal.2012003tw369
{"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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