最近、DrosophilaでScienceとNat Immunolが出た↓
Essential function in vivo for Dicer-2 in host defense against RNA viruses in drosophila.
Galiana-Arnoux D, Dostert C, Schneemann A, Hoffmann JA, Imler JL.
Nat Immunol. 2006 Jun;7(6):590-7. Epub 2006 Mar 23.
http://
RNA interference directs innate immunity against viruses in adult Drosophila.
Wang XH, Aliyari R, Li WX, Li HW, Kim K, Carthew R, Atkinson P, Ding SW.
Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.
http://
Animal virus replication and RNAi-mediated antiviral silencing in Caenorhabditis elegans.
Lu R, Maduro M, Li F, Li HW, Broitman-Maduro G, Li WX, Ding SW.
Nature. 2005 Aug 18;436(7053):1040-3.
http://
Evidence that HIV-1 encodes an siRNA and a suppressor of RNA silencing.
Bennasser Y, Le SY, Benkirane M, Jeang KT.
Immunity. 2005 May;22(5):607-19. Erratum in: Immunity. 2005 Jun;22(6):773.
http://
Essential function in vivo for Dicer-2 in host defense against RNA viruses in drosophila.
Galiana-Arnoux D, Dostert C, Schneemann A, Hoffmann JA, Imler JL.
Nat Immunol. 2006 Jun;7(6):590-7. Epub 2006 Mar 23.
http://
RNA interference directs innate immunity against viruses in adult Drosophila.
Wang XH, Aliyari R, Li WX, Li HW, Kim K, Carthew R, Atkinson P, Ding SW.
Science. 2006 Apr 21;312(5772):452-4. Epub 2006 Mar 23.
http://
Animal virus replication and RNAi-mediated antiviral silencing in Caenorhabditis elegans.
Lu R, Maduro M, Li F, Li HW, Broitman-Maduro G, Li WX, Ding SW.
Nature. 2005 Aug 18;436(7053):1040-3.
http://
Evidence that HIV-1 encodes an siRNA and a suppressor of RNA silencing.
Bennasser Y, Le SY, Benkirane M, Jeang KT.
Immunity. 2005 May;22(5):607-19. Erratum in: Immunity. 2005 Jun;22(6):773.
http://
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コメント(8)
今日出たNat Immunolにreviewが載っている↓
Perspective
Nature Immunology 7, 563 - 567 (2006)
Published online: 19 May 2006; | doi:10.1038/ni1352
Is RNA interference involved in intrinsic antiviral immunity in mammals?
Bryan R Cullen
Bryan R. Cullen is with the Center for Virology and Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
RNA interference constitutes a key component of the innate immune response to viral infection in both plants and invertebrate animals and has been postulated to have a similar protective function in mammals. This perspective reviews the available data addressing whether RNA interference forms part of the mammalian innate immune response and concludes that the popular hypothesis in favor of that possibility remains far from proven and may not be valid.
http://www.nature.com/ni/journal/v7/n6/full/ni1352.html
Perspective
Nature Immunology 7, 563 - 567 (2006)
Published online: 19 May 2006; | doi:10.1038/ni1352
Is RNA interference involved in intrinsic antiviral immunity in mammals?
Bryan R Cullen
Bryan R. Cullen is with the Center for Virology and Department of Molecular Genetics and Microbiology, Duke University Medical Center, Durham, North Carolina 27710, USA.
RNA interference constitutes a key component of the innate immune response to viral infection in both plants and invertebrate animals and has been postulated to have a similar protective function in mammals. This perspective reviews the available data addressing whether RNA interference forms part of the mammalian innate immune response and concludes that the popular hypothesis in favor of that possibility remains far from proven and may not be valid.
http://www.nature.com/ni/journal/v7/n6/full/ni1352.html
Trends Immunolにも紹介されていた↓
Interfering antiviral immunity: application, subversion, hope?
Manjunath N, Kumar P, Lee SK, Shankar P.
Trends Immunol. 2006 Jun 3; [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16753342&query_hl=21&itool=pubmed_docsum
Interfering antiviral immunity: application, subversion, hope?
Manjunath N, Kumar P, Lee SK, Shankar P.
Trends Immunol. 2006 Jun 3; [Epub ahead of print]
http://www.ncbi.nlm.nih.gov/entrez/query.fcgi?db=pubmed&cmd=Retrieve&dopt=Abstract&list_uids=16753342&query_hl=21&itool=pubmed_docsum
Originally published in Science Express on 1 June 2006
Science 7 July 2006:
Vol. 313. no. 5783, pp. 68 - 71
http://www.sciencemag.org/cgi/content/abstract/313/5783/68?etoc
Research Articles
Hierarchical Action and Inhibition of Plant Dicer-Like Proteins in Antiviral Defense
Ang?lique Deleris,1 Javier Gallego-Bartolome,1 Jinsong Bao,2 Kristin D. Kasschau,2 James C. Carrington,2 Olivier Voinnet1*
The mechanisms underlying induction and suppression of RNA silencing in the ongoing plant-virus arms race are poorly understood. We show here that virus-derived small RNAs produced by Arabidopsis Dicer-like 4 (DCL4) program an effector complex conferring antiviral immunity. Inhibition of DCL4 by a viral-encoded suppressor revealed the subordinate antiviral activity of DCL2. Accordingly, inactivating both DCL2 and DCL4 was necessary and sufficient to restore systemic infection of a suppressor-deficient virus. The effects of DCL2 were overcome by increasing viral dosage in inoculated leaves, but this could not surmount additional, non?cell autonomous effects of DCL4 specifically preventing viral unloading from the vasculature. These findings define a molecular framework for studying antiviral silencing and defense in plants.
1 Institut de Biologie Mol?culaire des Plantes, CNRS Unit? Propre de Recherche (UPR) 2357, 12, rue du G?n?ral Zimmer, 67084 Strasbourg Cedex, France.
2 Center for Genome Research and Biocomputing, Oregon State University, Corvallis, OR 97331, USA.
Science 7 July 2006:
Vol. 313. no. 5783, pp. 68 - 71
http://www.sciencemag.org/cgi/content/abstract/313/5783/68?etoc
Research Articles
Hierarchical Action and Inhibition of Plant Dicer-Like Proteins in Antiviral Defense
Ang?lique Deleris,1 Javier Gallego-Bartolome,1 Jinsong Bao,2 Kristin D. Kasschau,2 James C. Carrington,2 Olivier Voinnet1*
The mechanisms underlying induction and suppression of RNA silencing in the ongoing plant-virus arms race are poorly understood. We show here that virus-derived small RNAs produced by Arabidopsis Dicer-like 4 (DCL4) program an effector complex conferring antiviral immunity. Inhibition of DCL4 by a viral-encoded suppressor revealed the subordinate antiviral activity of DCL2. Accordingly, inactivating both DCL2 and DCL4 was necessary and sufficient to restore systemic infection of a suppressor-deficient virus. The effects of DCL2 were overcome by increasing viral dosage in inoculated leaves, but this could not surmount additional, non?cell autonomous effects of DCL4 specifically preventing viral unloading from the vasculature. These findings define a molecular framework for studying antiviral silencing and defense in plants.
1 Institut de Biologie Mol?culaire des Plantes, CNRS Unit? Propre de Recherche (UPR) 2357, 12, rue du G?n?ral Zimmer, 67084 Strasbourg Cedex, France.
2 Center for Genome Research and Biocomputing, Oregon State University, Corvallis, OR 97331, USA.
A role for Dicer in immune regulation
http://www.jem.org/cgi/content/abstract/203/11/2519
Bradley S. Cobb1, Arnulf Hertweck1, James Smith4, Eric O'Connor3, Daniel Graf6, Terence Cook2, Stephen T. Smale7, Shimon Sakaguchi8, Frederick J. Livesey4,5, Amanda G. Fisher1, and Matthias Merkenschlager1
1 Lymphocyte Development Group, 2 Division of Investigative Sciences, and 3 Flow Cytometry Facility, MRC Clinical Sciences Centre, Imperial College London, London W12 0NN, England, UK
4 Wellcome Trust/CRUK Gurdon Institute and 5 Department of Biochemistry, University of Cambridge, Cambridge CB2 1QN, England, UK
6 Institute of Immunology, Biomedical Sciences Research Center "Al. Fleming," 166 72 Vari, Greece
7 Department of Microbiology, Immunology, and Molecular Genetics, and Molecular Biology Institute, University of California, Los Angeles, CA 90095
8 Department of Experimental Pathology, Institute for Frontier Medical Science, Kyoto University, Kyoto 606-8501, Japan
Micro RNAs (miRNAs) regulate gene expression at the posttranscriptional level. Here we show that regulatory T (T reg) cells have a miRNA profile distinct from conventional CD4 T cells. A partial T reg cell?like miRNA profile is conferred by the enforced expression of Foxp3 and, surprisingly, by the activation of conventional CD4 T cells. Depleting miRNAs by eliminating Dicer, the RNAse III enzyme that generates functional miRNAs, reduces T reg cell numbers and results in immune pathology. Dicer facilitates, in a cell-autonomous fashion, the development of T reg cells in the thymus and the efficient induction of Foxp3 by transforming growth factor ?. These results suggest that T reg cell development involves Dicer-generated RNAs.
http://www.jem.org/cgi/content/abstract/203/11/2519
Bradley S. Cobb1, Arnulf Hertweck1, James Smith4, Eric O'Connor3, Daniel Graf6, Terence Cook2, Stephen T. Smale7, Shimon Sakaguchi8, Frederick J. Livesey4,5, Amanda G. Fisher1, and Matthias Merkenschlager1
1 Lymphocyte Development Group, 2 Division of Investigative Sciences, and 3 Flow Cytometry Facility, MRC Clinical Sciences Centre, Imperial College London, London W12 0NN, England, UK
4 Wellcome Trust/CRUK Gurdon Institute and 5 Department of Biochemistry, University of Cambridge, Cambridge CB2 1QN, England, UK
6 Institute of Immunology, Biomedical Sciences Research Center "Al. Fleming," 166 72 Vari, Greece
7 Department of Microbiology, Immunology, and Molecular Genetics, and Molecular Biology Institute, University of California, Los Angeles, CA 90095
8 Department of Experimental Pathology, Institute for Frontier Medical Science, Kyoto University, Kyoto 606-8501, Japan
Micro RNAs (miRNAs) regulate gene expression at the posttranscriptional level. Here we show that regulatory T (T reg) cells have a miRNA profile distinct from conventional CD4 T cells. A partial T reg cell?like miRNA profile is conferred by the enforced expression of Foxp3 and, surprisingly, by the activation of conventional CD4 T cells. Depleting miRNAs by eliminating Dicer, the RNAse III enzyme that generates functional miRNAs, reduces T reg cell numbers and results in immune pathology. Dicer facilitates, in a cell-autonomous fashion, the development of T reg cells in the thymus and the efficient induction of Foxp3 by transforming growth factor ?. These results suggest that T reg cell development involves Dicer-generated RNAs.
Dicerではないが
Expression of artificial microRNAs in transgenic Arabidopsis thaliana confers virus resistance
Nat Biotechnol. 2006 Oct 22; [Epub ahead of print]
http://www.nature.com/nbt/journal/vaop/ncurrent/abs/nbt1255.html
Qi-Wen Niu1, 4, Shih-Shun Lin1, 4, Jose Luis Reyes1, 3, Kuan-Chun Chen1, 3, Hui-Wen Wu1, Shyi-Dong Yeh2 & Nam-Hai Chua1
1 Laboratory of Plant Molecular Biology, Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.
2 Department of Plant Pathology, National Chung Hsing University, 250 Kao Kung Road, Taichung, Taiwan 402.
3 Present addresses: Instituto de Biotecnolog?a-UNAM. Ave. Universidad 2001, Cuernavaca, Morelos 62215, Mexico (J.L.R.), Department of Plant Pathology, National Chung Hsing University, 250 Kao Kung Road, Taichung, Taiwan 402 (K.-C.C.).
4 These authors contributed equally to this work.
Plant microRNAs (miRNAs) regulate the abundance of target mRNAs by guiding their cleavage at the sequence complementary region. We have modified an Arabidopsis thaliana miR159 precursor to express artificial miRNAs (amiRNAs) targeting viral mRNA sequences encoding two gene silencing suppressors, P69 of turnip yellow mosaic virus (TYMV) and HC-Pro of turnip mosaic virus (TuMV). Production of these amiRNAs requires A. thaliana DICER-like protein 1. Transgenic A. thaliana plants expressing amiR-P69159 and amiR-HC-Pro159 are specifically resistant to TYMV and TuMV, respectively. Expression of amiR-TuCP159 targeting TuMV coat protein sequences also confers specific TuMV resistance. However, transgenic plants that express both amiR-P69159 and amiR-HC-Pro159 from a dimeric pre-amiR-P69159/amiR-HC-Pro159 transgene are resistant to both viruses. The virus resistance trait is displayed at the cell level and is hereditable. More important, the resistance trait is maintained at 15 °C, a temperature that compromises small interfering RNA?mediated gene silencing. The amiRNA-mediated approach should have broad applicability for engineering multiple virus resistance in crop plants.
Expression of artificial microRNAs in transgenic Arabidopsis thaliana confers virus resistance
Nat Biotechnol. 2006 Oct 22; [Epub ahead of print]
http://www.nature.com/nbt/journal/vaop/ncurrent/abs/nbt1255.html
Qi-Wen Niu1, 4, Shih-Shun Lin1, 4, Jose Luis Reyes1, 3, Kuan-Chun Chen1, 3, Hui-Wen Wu1, Shyi-Dong Yeh2 & Nam-Hai Chua1
1 Laboratory of Plant Molecular Biology, Rockefeller University, 1230 York Avenue, New York, New York 10021, USA.
2 Department of Plant Pathology, National Chung Hsing University, 250 Kao Kung Road, Taichung, Taiwan 402.
3 Present addresses: Instituto de Biotecnolog?a-UNAM. Ave. Universidad 2001, Cuernavaca, Morelos 62215, Mexico (J.L.R.), Department of Plant Pathology, National Chung Hsing University, 250 Kao Kung Road, Taichung, Taiwan 402 (K.-C.C.).
4 These authors contributed equally to this work.
Plant microRNAs (miRNAs) regulate the abundance of target mRNAs by guiding their cleavage at the sequence complementary region. We have modified an Arabidopsis thaliana miR159 precursor to express artificial miRNAs (amiRNAs) targeting viral mRNA sequences encoding two gene silencing suppressors, P69 of turnip yellow mosaic virus (TYMV) and HC-Pro of turnip mosaic virus (TuMV). Production of these amiRNAs requires A. thaliana DICER-like protein 1. Transgenic A. thaliana plants expressing amiR-P69159 and amiR-HC-Pro159 are specifically resistant to TYMV and TuMV, respectively. Expression of amiR-TuCP159 targeting TuMV coat protein sequences also confers specific TuMV resistance. However, transgenic plants that express both amiR-P69159 and amiR-HC-Pro159 from a dimeric pre-amiR-P69159/amiR-HC-Pro159 transgene are resistant to both viruses. The virus resistance trait is displayed at the cell level and is hereditable. More important, the resistance trait is maintained at 15 °C, a temperature that compromises small interfering RNA?mediated gene silencing. The amiRNA-mediated approach should have broad applicability for engineering multiple virus resistance in crop plants.
Retraction
Anti-apoptotic function of a microRNA encoded by the HSV-1 latency-associated transcript
A. Gupta, J. J. Gartner, P. Sethupathy, A. G. Hatzigeorgiou & N. W. Fraser
Nature 442, 82–85 (2006)
We claimed that there was a microRNA in the exon 1 region of the latency-associated transcript of herpes simplex virus-1 (HSV-1) that downregulated the expression of transforming growth factor- (TGF-). We postulated that through this mechanism the virus prevented the latently infected cell from apoptosing. We are confident that HSV-1 downregulates TGFB messenger RNA; however, the mapping of this downregulation to the region of the HSV-1 genome that we predicted to encode the microRNA is not supported by further experiments in several laboratories.
B. R. Cullen from Duke University and D. Coen from Harvard University have not been able to detect the microRNA that we described. Using samples that they have supplied, we also been unable to consistently detect the predicted microRNA. Furthermore, in the samples supplied by the Cullen laboratory, we could only detect miR-LAT signal in SY5Y neuronal-like cell samples and not in non-neuronal 293 cell samples. The SY5Y cells were found to be positive for miR-LAT, regardless of whether or not they were infected with HSV-1, suggesting that we are detecting a SY5Y-encoded microRNA.
A.G. has declined to sign the retraction because she maintains that the original observations are correct.
http://www.nature.com/nature/journal/v451/n7178/full/nature06621.html
Anti-apoptotic function of a microRNA encoded by the HSV-1 latency-associated transcript
A. Gupta, J. J. Gartner, P. Sethupathy, A. G. Hatzigeorgiou & N. W. Fraser
Nature 442, 82–85 (2006)
We claimed that there was a microRNA in the exon 1 region of the latency-associated transcript of herpes simplex virus-1 (HSV-1) that downregulated the expression of transforming growth factor- (TGF-). We postulated that through this mechanism the virus prevented the latently infected cell from apoptosing. We are confident that HSV-1 downregulates TGFB messenger RNA; however, the mapping of this downregulation to the region of the HSV-1 genome that we predicted to encode the microRNA is not supported by further experiments in several laboratories.
B. R. Cullen from Duke University and D. Coen from Harvard University have not been able to detect the microRNA that we described. Using samples that they have supplied, we also been unable to consistently detect the predicted microRNA. Furthermore, in the samples supplied by the Cullen laboratory, we could only detect miR-LAT signal in SY5Y neuronal-like cell samples and not in non-neuronal 293 cell samples. The SY5Y cells were found to be positive for miR-LAT, regardless of whether or not they were infected with HSV-1, suggesting that we are detecting a SY5Y-encoded microRNA.
A.G. has declined to sign the retraction because she maintains that the original observations are correct.
http://www.nature.com/nature/journal/v451/n7178/full/nature06621.html
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