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Citation: Cullen BR (2013) How Do Viruses Avoid Inhibition by Endogenous Cellular MicroRNAs? PLoS Pathog 9(11): e1003694. doi:10.1371/journal.ppat.1003694
Editor: Richard C. Condit, University of Florida, United States of America
Published: November 7, 2013
Copyright: ? 2013 Cullen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by National Institutes of Health research grants R01-DA030086 and R01-AI067968. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The author has declared that no competing interests exist.
Introduction
MicroRNAs (miRNAs) are an extensive family of small regulatory RNAs that function by binding to complementary mRNAs, primarily in the 3′ untranslated region (3′UTRs), and then inhibiting their expression by reducing mRNA translation and/or stability [1]. MiRNAs are initially transcribed as long pri-miRNAs, which are sequentially processed by the RNase III enzymes Drosha, in the nucleus, and Dicer, in the cytoplasm, to generate the mature, ~22-nt miRNA [2]. This is then loaded into the RNA Induced Silencing Complex (RISC), which consists minimally of one of the four mammalian Argonaut proteins, Ago1 to Ago4, as well as a member of the GW182 protein family. MiRNAs function as guide RNAs to target RISC to complementary mRNA sequences on specific mRNA 3′UTRs. Analysis has revealed that complementarity to nucleotides 2 through 8 of the miRNA, the so-called seed region, is particularly important for effective RISC recruitment [1], although non-canonical sites, with incomplete seed complementarity, have also been reported [3]. Importantly, RISC recruitment to target sites that are occluded by RNA secondary structure or bound proteins is very inefficient [4].
full article
http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003694
Editor: Richard C. Condit, University of Florida, United States of America
Published: November 7, 2013
Copyright: ? 2013 Cullen. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: This work was supported by National Institutes of Health research grants R01-DA030086 and R01-AI067968. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Competing interests: The author has declared that no competing interests exist.
Introduction
MicroRNAs (miRNAs) are an extensive family of small regulatory RNAs that function by binding to complementary mRNAs, primarily in the 3′ untranslated region (3′UTRs), and then inhibiting their expression by reducing mRNA translation and/or stability [1]. MiRNAs are initially transcribed as long pri-miRNAs, which are sequentially processed by the RNase III enzymes Drosha, in the nucleus, and Dicer, in the cytoplasm, to generate the mature, ~22-nt miRNA [2]. This is then loaded into the RNA Induced Silencing Complex (RISC), which consists minimally of one of the four mammalian Argonaut proteins, Ago1 to Ago4, as well as a member of the GW182 protein family. MiRNAs function as guide RNAs to target RISC to complementary mRNA sequences on specific mRNA 3′UTRs. Analysis has revealed that complementarity to nucleotides 2 through 8 of the miRNA, the so-called seed region, is particularly important for effective RISC recruitment [1], although non-canonical sites, with incomplete seed complementarity, have also been reported [3]. Importantly, RISC recruitment to target sites that are occluded by RNA secondary structure or bound proteins is very inefficient [4].
full article
http://www.plospathogens.org/article/info:doi/10.1371/journal.ppat.1003694