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microRNAs (miRNAs) encode a novel class of small, non-coding RNAs that regulate gene expression post-trancriptionally. miRNAs
comprise one of the major non-coding RNA families, whose diverse biological functions and unusual capacity for gene regulation
have attracted enormous interests in the RNA world. Over the past 16 years, genetic, biochemical and computational approaches
have greatly shaped the growth of the field, leading to the identification of thousands of miRNA genes in nearly all metazoans.
The key molecular machinery for miRNA biogenesis and silencing has been identified, yet the precise biochemical and regulatory
mechanisms still remain elusive. However, recent findings have shed new light on how miRNAs are generated and how they function
to repress gene expression. miRNAs provide a paradigm for endogenous small RNAs that mediate gene silencing at a genome-wide
level. The gene silencing mediated by these small RNAs constitutes a major component of gene regulation during various developmental
and physiological processes. The accumulating knowledge about their biogenesis and gene silencing mechanism will add a new
dimension to our understanding about the complex gene regulatory networks. 相似文献
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Herr AJ 《FEBS letters》2005,579(26):5879-5888
RNA silencing pathways in plants have diversified along with key gene families involved in small RNA biogenesis and effector steps. Evidence suggests that these pathways have distinct roles in plant biology. 相似文献
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Molecular aspects of malaria pathogenesis 总被引:4,自引:0,他引:4
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Much of what is known about antigenic variation in the human malaria parasite Plasmodium falciparum has been established by the study of phenotypic changes at the surface of parasitized red blood cells. Although this has contributed to our fundamental understanding of immune escape, nothing conclusive has been elucidated about the molecular mechanisms that determine activation and silencing of members of the antigenic variation var gene family. Recent findings indicate that reversible chromatin modifications and perinuclear gene movement are epigenetic factors that define the silent and active states of telomere-adjacent var genes. 相似文献
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Virus-induced gene silencing of argonaute genes in Nicotiana benthamiana demonstrates that extensive systemic silencing requires Argonaute1-like and Argonaute4-like genes
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Several distinct pathways of RNA silencing operate in plants with roles including the suppression of virus accumulation, control of endogenous gene expression, and direction of DNA and chromatin modifications. Proteins of the Dicer-Like and Argonaute (AGO) families have key roles within these silencing pathways and have distinct biochemical properties. We are interested in the relationships between different silencing pathways and have used Nicotiana benthamiana as a model system. While not being an amenable plant for traditional genetics, N. benthamiana is extensively used for RNA-silencing studies. Using virus-induced gene silencing technology we demonstrate that both NbAGO1- and NbAGO4-like genes are required for full systemic silencing but not for silencing directed by an inverted repeat transgene. Phenotypic differences between the virus-induced gene silencing plants indicate that NbAGO1 and NbAGO4 like act at different stages of the silencing pathways. Suppression of NbAGO1 expression recapitulated the hypomorphic mutant phenotype of certain Arabidopsis (Arabidopsis thaliana) ago1 alleles, however, suppression of NbAgo4 like resulted in phenotypes differing in some respects from those reported for Arabidopsis ago4. We suggest that the small interfering RNA amplification step required for full systemic silencing is dependent upon a nuclear event requiring the activity of NbAGO4 like. 相似文献
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Andrey Poleshko Andrew V Kossenkov Natalia Shalginskikh Anna Pecherskaya Anna Pecherskaya Margret B Einarson Margret B Einarson Anna Marie Skalka Anna Marie Skalka Richard A Katz Richard A Katz 《Epigenetics》2014,9(9):1280-1289
Cellular identity in both normal and disease processes is determined by programmed epigenetic activation or silencing of specific gene subsets. Here, we have used human cells harboring epigenetically silent GFP-reporter genes to perform a genome-wide siRNA knockdown screen for the identification of cellular factors that are required to maintain epigenetic gene silencing. This unbiased screen interrogated 21,121 genes, and we identified and validated a set of 128 protein factors. This set showed enrichment for functional categories, and protein-protein interactions. Among this set were known epigenetic silencing factors, factors with no previously identified role in epigenetic gene silencing, as well as unstudied factors. The set included non-nuclear factors, for example, components of the integrin-adhesome. A key finding was that the E1 and E2 enzymes of the small ubiquitin-like modifier (SUMO) pathway (SAE1, SAE2/UBA2, UBC9/UBE2I) are essential for maintenance of epigenetic silencing. This work provides the first genome-wide functional view of human factors that mediate epigenetic gene silencing. The screen output identifies novel epigenetic factors, networks, and mechanisms, and provides a set of candidate targets for epigenetic therapy and cellular reprogramming. 相似文献
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《Epigenetics》2013,8(9):1280-1289
Cellular identity in both normal and disease processes is determined by programmed epigenetic activation or silencing of specific gene subsets. Here, we have used human cells harboring epigenetically silent GFP-reporter genes to perform a genome-wide siRNA knockdown screen for the identification of cellular factors that are required to maintain epigenetic gene silencing. This unbiased screen interrogated 21,121 genes, and we identified and validated a set of 128 protein factors. This set showed enrichment for functional categories, and protein-protein interactions. Among this set were known epigenetic silencing factors, factors with no previously identified role in epigenetic gene silencing, as well as unstudied factors. The set included non-nuclear factors, for example, components of the integrin-adhesome. A key finding was that the E1 and E2 enzymes of the small ubiquitin-like modifier (SUMO) pathway (SAE1, SAE2/UBA2, UBC9/UBE2I) are essential for maintenance of epigenetic silencing. This work provides the first genome-wide functional view of human factors that mediate epigenetic gene silencing. The screen output identifies novel epigenetic factors, networks, and mechanisms, and provides a set of candidate targets for epigenetic therapy and cellular reprogramming. 相似文献
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Xenogeneic silencing proteins facilitate horizontal gene transfer by silencing expression of AT-rich sequences. By virtue of their activity these proteins serve as master regulators of a variety of important functions including motility, drug resistance, and virulence. Three families of silencers have been identified to date: the H-NS like proteins of Gram-negative bacteria, the MvaT like proteins of Pseudomonacae, and the Lsr2 proteins of Actinobacteria. Structural and biochemical characterization of these proteins have revealed that they share surprising commonalities in mechanism and function despite extensive divergence in both sequence and structure. Here we discuss the mechanisms that underlie the ability of these proteins to selectively target AT-rich DNA and the contradictory data regarding the mode by which H-NS forms nucleoprotein complexes. 相似文献
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Mechanisms underlying mutually exclusive expression of virulence genes by malaria parasites 总被引:4,自引:0,他引:4
Dzikowski R Li F Amulic B Eisberg A Frank M Patel S Wellems TE Deitsch KW 《EMBO reports》2007,8(10):959-965
A fundamental yet poorly understood aspect of gene regulation in eukaryotic organisms is the mechanisms that control allelic exclusion and mutually exclusive gene expression. In the malaria parasite Plasmodium falciparum, this process regulates expression of the var gene family--a large, hypervariable repertoire of genes that are responsible for the ability of the parasite to evade the host immune system and for pathogenesis of the disease. A central problem in understanding this process concerns the mechanisms that limit expression to a single gene at a time. Here, we describe results that provide information on the mechanisms that control silencing and single gene expression and differentiate between several models that have recently been proposed. The results provide the first evidence, to our knowledge, supporting the existence of a postulated var-specific, subnuclear expression site and also reinforce the conclusion that var gene regulation is based on cooperative interactions between the two promoters of each var gene. 相似文献