Science's STKEPub Date : 2002-08-20DOI: 10.1126/scisignal.1462002tw309
{"title":"The Ups and Downs of Expression","authors":"","doi":"10.1126/scisignal.1462002tw309","DOIUrl":"https://doi.org/10.1126/scisignal.1462002tw309","url":null,"abstract":"Gene expression varies substantially from one cell to another and depending on the history of the cell, its interactions, the state of its regulatory machinery, and so on. Elowitz et al. (see the Perspective by Fedoroff and Fontana) have focused on the noise in gene expression that is left when all other regulatory influences are equal. To measure this \"intrinsic noise,\" they used strains of Escherichia coli in which two alleles encoding distinguishable green fluorescent proteins were controlled by identical promoters. In these single bacterial cells, genes have essentially the same intracellular environment, so the variation in their expression is a measure of intrinsic noise. Intrinsic noise accounted for a substantial amount of the total variation in gene expression, and amount of noise varied with changes in other factors like transcription rate. M. B. Elowitz, A. J. Levine, E. D. Siggia, P. S. Swain, Stochastic gene expression in a single cell, Science 297, 1183-1186 (2002). [Abstract] [Full Text] N. Fedoroff, W. Fontana, Small numbers of big molecules, Science 297, 1129-1131 (2002). [Summary] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"236 1","pages":"tw309 - tw309"},"PeriodicalIF":0.0,"publicationDate":"2002-08-20","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"75012461","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 : 2002-08-13DOI: 10.1126/scisignal.1452002tw301
{"title":"Maintaining Immunity","authors":"","doi":"10.1126/scisignal.1452002tw301","DOIUrl":"https://doi.org/10.1126/scisignal.1452002tw301","url":null,"abstract":"Phosphoinositide 3-kinase activity regulates many cell processes across many cell types. There are three isoforms of its catalytic subunit p110, but their specificity has not been clear. Okkenhaug et al. generated a mouse that expresses an inactive form of p110 and observed compromised B and T cell immune function. The study reveals a highly selective, nonredundant role for this isoform in lymphocyte antigen receptor signaling, as well as a drug-development target. K. Okkenhaug, A. Bilancio, G. Farjot, H. Priddle, S. Sancho, E. Peskett, W. Pearce, S. E. Meek, A. Salpekar, M. D. Waterfield, A. J. H. Smith, B. Vanhaesebroeck, Impaired B and T cell antigen receptor signaling in p110δ PI 3-kinase mutant mice, Science 297, 1031-1034 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"39 1","pages":"TW301 - tw301"},"PeriodicalIF":0.0,"publicationDate":"2002-08-13","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"80866844","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 : 2002-08-06DOI: 10.1126/scisignal.1442002tw287
{"title":"Elements of a Fungal Light Receptor","authors":"","doi":"10.1126/scisignal.1442002tw287","DOIUrl":"https://doi.org/10.1126/scisignal.1442002tw287","url":null,"abstract":"The fungus Neurospora crassa is a light-sensitive organism, but its photoreceptor has remained elusive. The prime candidate, a transcription factor called White Collar-1 (WC-1), is required for all responses to light (see the Perspective by Linden). By eliminating the part of the WC-1 protein that would be expected to bind a chromophore (the LOV, or light, oxygen, and voltage, domain), He et al. show that the LOV domain is required for light responses, but not for the circadian clock function of WC-1. They then identify flavin adenine dinucleotide (FAD) as the chromophore bound to WC-1. Froehlich et al. show that WC-1 acts (as a dimer with WC-2) on two light-responsive elements in the promoter of the clock component frequency (FRQ). By reassembling this system in vitro and inducing FRQ transcription with light, these authors show that WC-1 is the blue light photoreceptor for Neurospora. In their system as well, FAD must be added in order to observe light reception. H. Linden, A white collar protein senses blue light, Science 297, 777-778 (2002). [Summary] [Full Text] He, P. Cheng, Y. Yang, L. Wang, K. H. Gardner, Y. Liu, White Collar-1, a DNA binding transcription factor and a light sensor, Science 297, 840-843 (2002). [Abstract] [Full Text] C. Froehlich, Y. Liu, J. J. Loros, J. C. Dunlap, White Collar-1, a circadian blue light photoreceptor, binding to the frequency promoter, Science 297, 815-819 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"37 12 1","pages":"TW287 - tw287"},"PeriodicalIF":0.0,"publicationDate":"2002-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"84969742","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 : 2002-08-06DOI: 10.1126/scisignal.1442002tw291
Sherri Koucky, A. Higgins
{"title":"FISH and Chips","authors":"Sherri Koucky, A. Higgins","doi":"10.1126/scisignal.1442002tw291","DOIUrl":"https://doi.org/10.1126/scisignal.1442002tw291","url":null,"abstract":"How do gene expression patterns change when a cell is perturbed, for example, by exposure to a pathogen or a drug? Although current chip-based methods of transcriptional profiling have provided researchers with a powerful tool for addressing this question, these methods require disruption of cellular architecture, meaning that important information may be lost. By combining elements of fluorescence in situ hybridization (FISH) and microarray technology, Levsky et al. have developed a technique that allows them to visualize the transcription of many genes simultaneously inside a single cell--essentially using the cell nucleus as a \"chip.\" J. M. Levsky, S. M. Shenoy, R. C. Pezo, R. H. Singer, Single-Cell gene expression profiling, Science 297, 836-840 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"15 1","pages":"TW291 - tw291"},"PeriodicalIF":0.0,"publicationDate":"2002-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86617193","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 : 2002-08-06DOI: 10.1126/scisignal.1442002tw290
{"title":"Viral Tricks","authors":"","doi":"10.1126/scisignal.1442002tw290","DOIUrl":"https://doi.org/10.1126/scisignal.1442002tw290","url":null,"abstract":"Herpesviruses replicate in the nucleus of host cells, but the particles formed are too big to pass through nuclear pores. How do they escape? Muranyi et al. (see the Perspective by Sanchez and Spector) found that murine cytomegalovirus subverts the normal activity of a cellular protein to aid its escape. A pair of viral proteins (M50/p35 and M53/p38) form a \"docking station\" for the viral capsids on the inner nuclear membrane. M50/p35 then recruits cellular protein kinase C to phosphorylate and disassemble the filamentous protein network of the nuclear lamina. W. Muranyi, J. Haas, M. Wagner, G. Krohne, U. H. Koszinowski, Cytomegalovirus recruitment of cellular kinases to dissolve the nuclear lamina, Science 297, 854-857 (2002). [Abstract] [Full Text] V. Sanchez, D. H. Spector, CMV makes a timely exit, Science 297, 778-779 (2002). [Summary] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"32 1","pages":"TW290 - tw290"},"PeriodicalIF":0.0,"publicationDate":"2002-08-06","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"86173466","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 : 2002-07-23DOI: 10.1126/scisignal.1422002tw268
{"title":"Staying Put","authors":"","doi":"10.1126/scisignal.1422002tw268","DOIUrl":"https://doi.org/10.1126/scisignal.1422002tw268","url":null,"abstract":"A large number of B cells inhabit the marginal zones (MZ) of the spleen, where they maintain steady contact with recirculating antigens in the blood. These lymphocytes respond rapidly to bacteria by mobilizing and differentiating into extensive clusters of antibody-producing plasma cells. Lu et al. show that two integrins involved in lymphocyte trafficking across endothelium, LFA-1 and α4β1, appear to be responsible for the migration and localization of MZ B cells. Large-scale egress of B cells from the MZ occurred when interactions of these integrins with their respective ligands were blocked. The retention of lymphocytes within lymphoid niches suggests a wider role for some integrins associated with lymphocyte trafficking. T. T. Lu, J. G. Cyster, Integrin-mediated long-term B cell retention in the splenic marginal zone, Science 297, 409-412 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"87 1","pages":"TW268 - TW268"},"PeriodicalIF":0.0,"publicationDate":"2002-07-23","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"82881097","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 : 2002-07-16DOI: 10.1126/scisignal.1412002tw252
{"title":"The Bloom in Spring","authors":"","doi":"10.1126/scisignal.1412002tw252","DOIUrl":"https://doi.org/10.1126/scisignal.1412002tw252","url":null,"abstract":"Vernalization, the coordinating of flowering with springtime, allows plants to accelerate flowering once the cold of winter is past. Levy et al. have now identified one of the molecular regulators of the vernalization response in the small flowering plant Arabidopsis. VRN1 is a DNA-binding protein that helps keep a floral repressor molecule out of action and allows flowering to proceed. VRN1 also shows an intriguing propensity to alter flowering time without working through this particular floral repressor, which suggests that floral initiation integrates inputs from multiple pathways. Y. Y. Levy, S. Mesnage, J. S. Mylne, A. R. Gendall, C. Dean, Multiple roles of Arabidopsis VRN1 in vernalization and flowering time control. Science 297, 243-246 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"52 3","pages":"tw252 - tw252"},"PeriodicalIF":0.0,"publicationDate":"2002-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"91438376","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 : 2002-07-16DOI: 10.1126/science.297.5579.153k
{"title":"The Legwork of Signaling","authors":"","doi":"10.1126/science.297.5579.153k","DOIUrl":"https://doi.org/10.1126/science.297.5579.153k","url":null,"abstract":"The fruit fly leg is a complex structure with 10 segments. Studies of Drosophila appendage development have identified several of the components that are needed to establish the dorsal-ventral (DV) and the proximal-distal (PD) axes of the leg. Signaling by wingless (wg) and decapentaplegic (dpp) operate in the developmental program for both of these axes. However, genetics studies by Galindo et al. show that wg and dpp are not sufficient to explain all of the subsequent patterning events in the PD axis. The tarsus segment, an evolutionarily ancient part of the insect leg, is defined by a dpp/wg-independent phase of distalless and dachshund activity combined with a distal gradient of epidermal growth factor receptor-Ras signaling. M. I. Galindo, S. A. Bishop, S. Greig, J. P. Couso, Leg patterning driven by proximal-distal interactions and EGFR signaling. Science 297, 256-259 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"22 1","pages":"tw253 - tw253"},"PeriodicalIF":0.0,"publicationDate":"2002-07-16","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"73766002","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 : 2002-07-09DOI: 10.1126/scisignal.1402002tw243
{"title":"An On/Off Switch for Oncogenes","authors":"","doi":"10.1126/scisignal.1402002tw243","DOIUrl":"https://doi.org/10.1126/scisignal.1402002tw243","url":null,"abstract":"Among the many new strategies being developed for cancer therapy are drugs that inhibit the function of oncogenes that are involved in tumorigenesis. Such drugs might be toxic if used chronically, yet they might be ineffective in the short-term because of possible reactivation of the oncogene once treatment is stopped. To investigate the latter possibility, Jain et al. (see the Perspective by Weinstein) used a sophisticated mouse genetic model to examine what happens to MYC-induced tumors when the MYC oncogene is briefly inactivated and subsequently reactivated. Surprisingly, they found that transient MYC inactivation leads to permanent loss of the neoplastic phenotype. When MYC was removed, osteogenic sarcoma cells differentiated into bone cells; reexpression of MYC did not restore the cells' tumorigenic potential but rather caused the cells to undergo apoptosis. These results suggest that brief inactivation of an oncogene may permanently change the epigenetic context of a tumor cell so that it cannot revert to its original malignant behavior. M. Jain, C. Arvanitis, K. Chu, W. Dewey, E. Leonhardt, M. Trinh, C. D. Sundberg, J. M. Bishop, D. W. Felsher, Sustained loss of a neoplastic phenotype by brief interaction of MYC. Science 296, 102-104 (2002). [Abstract] [Full Text] I. B. Weinstein, Addiction to oncogenes - the Achilles heal of cancer. Science 297, 63-64 (2002). [Summary] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"2 1","pages":"TW243 - tw243"},"PeriodicalIF":0.0,"publicationDate":"2002-07-09","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"76141892","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 : 2002-07-02DOI: 10.1126/scisignal.1392002tw236
{"title":"Infection Protection During Inflammation","authors":"","doi":"10.1126/scisignal.1392002tw236","DOIUrl":"https://doi.org/10.1126/scisignal.1392002tw236","url":null,"abstract":"During microbial infection, neutrophils generate microbicidal agents through the release of myeloperoxidase (MPO). Eiserich et al. report that MPO's actions during inflammation extend beyond generating antimicrobial oxidizing species. MPO permeates the mammalian vasculature and alters blood vessel function during acute inflammation by catabolizing nitric oxide (NO). NO is an endothelial-derived blood vessel relaxant that is produced in response to endotoxin. By reducing NO availability, MPO impairs vascular changes produced by infection. This finding may explain the increased susceptibility of humans deficient in MPO to infection. J. P. Eiserich, S. Baldus, M.-L. Brennan, W. Ma, C. Zhang, A. Tousson, L. Castro, A. J. Lusis, W. M. Nauseef, C. R. White, B. A. Freeman, Myeloperoxidase, a leukocyte-derived vascular NO oxidase. Science 296, 2391-2394 (2002). [Abstract] [Full Text]","PeriodicalId":21619,"journal":{"name":"Science's STKE","volume":"34 1","pages":"TW236 - tw236"},"PeriodicalIF":0.0,"publicationDate":"2002-07-02","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":null,"resultStr":null,"platform":"Semanticscholar","paperid":"88284517","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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