The Experts below are selected from a list of 2901 Experts worldwide ranked by ideXlab platform
Mikiko C. Siomi - One of the best experts on this subject based on the ideXlab platform.
-
essential roles of windei and nuclear monoubiquitination of eggless setdb1 in Transposon Silencing
EMBO Reports, 2019Co-Authors: Ken Osumi, Haruhiko Siomi, Kaoru Sato, Kensaku Murano, Mikiko C. SiomiAbstract:: Eggless/SETDB1 (Egg), the only essential histone methyltransferase (HMT) in Drosophila, plays a role in gene repression, including piRNA-mediated Transposon Silencing in the ovaries. Previous studies suggested that Egg is post-translationally modified and showed that Windei (Wde) regulates Egg nuclear localization through protein-protein interaction. Monoubiquitination of mammalian SETDB1 is necessary for the HMT activity. Here, using cultured ovarian somatic cells, we show that Egg is monoubiquitinated and phosphorylated but that only monoubiquitination is required for piRNA-mediated Transposon repression. Egg monoubiquitination occurs in the nucleus. Egg has its own nuclear localization signal, and the nuclear import of Egg is Wde-independent. Wde recruits Egg to the chromatin at target gene Silencing loci, but their interaction is monoubiquitin-independent. The abundance of nuclear Egg is governed by that of nuclear Wde. These results illuminate essential roles of nuclear monoubiquitination of Egg and the role of Wde in piRNA-mediated Transposon repression.
-
Essential roles of Windei and nuclear monoubiquitination of Eggless/SETDB1 in Transposon Silencing.
EMBO reports, 2019Co-Authors: Ken Osumi, Haruhiko Siomi, Kaoru Sato, Kensaku Murano, Mikiko C. SiomiAbstract:Eggless/SETDB1 (Egg), the only essential histone methyltransferase (HMT) in Drosophila, plays a role in gene repression, including piRNA-mediated Transposon Silencing in the ovaries. Previous studies suggested that Egg is post-translationally modified and showed that Windei (Wde) regulates Egg nuclear localization through protein-protein interaction. Monoubiquitination of mammalian SETDB1 is necessary for the HMT activity. Here, using cultured ovarian somatic cells, we show that Egg is monoubiquitinated and phosphorylated but that only monoubiquitination is required for piRNA-mediated Transposon repression. Egg monoubiquitination occurs in the nucleus. Egg has its own nuclear localization signal, and the nuclear import of Egg is Wde-independent. Wde recruits Egg to the chromatin at target gene Silencing loci, but their interaction is monoubiquitin-independent. The abundance of nuclear Egg is governed by that of nuclear Wde. These results illuminate essential roles of nuclear monoubiquitination of Egg and the role of Wde in piRNA-mediated Transposon repression.
-
Requirements for multivalent Yb body assembly in Transposon Silencing in Drosophila
EMBO reports, 2019Co-Authors: Shigeki Hirakata, Hirotsugu Ishizu, Aoi Fujita, Yumiko Tomoe, Mikiko C. SiomiAbstract:Abstract Female sterile (1) Yb (Yb) is a primary component of Yb bodies, perinuclear foci considered to be the site of PIWI‐interacting RNA (piRNA) biogenesis in Drosophila ovarian somatic cells (OSCs). Yb consists of three domains: Helicase C‐terminal (Hel‐C), RNA helicase, and extended Tudor (eTud) domains. We previously showed that the RNA helicase domain is necessary for Yb–RNA interaction, Yb body formation, and piRNA biogenesis. Here, we investigate the functions of Hel‐C and eTud and reveal that Hel‐C is dedicated to Yb–Yb homotypic interaction, while eTud is necessary for Yb–RNA association, as is the RNA helicase domain. All of these domains are indispensable for Yb body formation and Transposon‐repressing piRNA production. Strikingly, however, genic piRNAs unrelated to Transposon Silencing are produced in OSCs where Yb bodies are disassembled. We also reveal that Yb bodies are liquid‐like multivalent condensates whose assembly depends on Yb–Yb homotypic interaction and Yb binding particularly with flamenco RNA transcripts, the source of Transposon‐repressing piRNAs. New insights into Yb body assembly and biological relevance of Yb bodies in Transposon Silencing have emerged.
-
inheritance of a nuclear piwi from pluripotent stem cells by somatic descendants ensures differentiation by Silencing Transposons in planarian
Developmental Cell, 2016Co-Authors: Norito Shibata, Haruhiko Siomi, Kuniaki Saito, Makoto Kashima, Taisuke Ishiko, Osamu Nishimura, Labib Rouhana, Kazuyo Misaki, Shigenobu Yonemura, Mikiko C. SiomiAbstract:Differentiation of pluripotent stem cells (PSCs) requires Transposon Silencing throughout the process. PIWIs, best known as key factors in germline Transposon Silencing, are also known to act in somatic differentiation of planarian PSCs (neoblasts). However, how PIWIs control the latter process remains elusive. Here, using Dugesia japonica, we show that a nuclear PIWI, DjPiwiB, was bound to PIWI-interacting RNAs (generally key mediators of PIWI-dependent Transposon Silencing), and was detected in not only neoblasts but also their descendant somatic cells, which do not express piwi. In contrast, cytoplasmic DjPiwiA and DjPiwiC were detected only in neoblasts, in accord with their transcription there. DjPiwiB was indispensable for regeneration, but dispensable for Transposon Silencing in neoblasts. However, Transposons were derepressed at the onset of differentiation in DjPiwiB-knockdown planarians. Thus, DjPiwiB appears to be inherited by descendant somatic cells of neoblasts to ensure Transposon Silencing in those cells, which are unable to produce PIWI proteins.
-
crystal structure and activity of the endoribonuclease domain of the pirna pathway factor maelstrom
Cell Reports, 2015Co-Authors: Naoki Matsumoto, Haruhiko Siomi, Kaoru Sato, Hiroshi Nishimasu, Yurika Namba, Kana Miyakubi, Naoshi Dohmae, Ryuichiro Ishitani, Mikiko C. SiomiAbstract:PIWI-interacting RNAs (piRNAs) protect the genome from Transposons in animal gonads. Maelstrom (Mael) is an evolutionarily conserved protein, composed of a high-mobility group (HMG) domain and a MAEL domain, and is essential for piRNA-mediated transcriptional Transposon Silencing in various species, such as Drosophila and mice. However, its structure and biochemical function have remained elusive. Here, we report the crystal structure of the MAEL domain from Drosophila melanogaster Mael, at 1.6 A resolution. The structure reveals that the MAEL domain has an RNase H-like fold but lacks canonical catalytic residues conserved among RNase H-like superfamily nucleases. Our biochemical analyses reveal that the MAEL domain exhibits single-stranded RNA (ssRNA)-specific endonuclease activity. Our cell-based analyses further indicate that ssRNA cleavage activity appears dispensable for piRNA-mediated transcriptional Transposon Silencing in Drosophila. Our findings provide clues toward understanding the multiple roles of Mael in the piRNA pathway.
Tao Cai - One of the best experts on this subject based on the ideXlab platform.
-
the rna surveillance complex pelo hbs1 is required for Transposon Silencing in the drosophila germline
EMBO Reports, 2015Co-Authors: Fu Yang, Rui Zhao, Xiaofeng Fang, Huanwei Huang, Yang Xuan, Hongyan Chen, Tao CaiAbstract:Abstract Silencing of transposable elements (TEs) in the metazoan germline is critical for genome integrity and is primarily dependent on Piwi proteins and associated RNAs, which exert their function through both transcriptional and posttranscriptional mechanisms. Here, we report that the evolutionarily conserved Pelo (Dom34)‐Hbs1 mRNA surveillance complex is required for Transposon Silencing in the Drosophila germline. In pelo mutant gonads, mRNAs and proteins of some selective TEs are up‐regulated. Pelo is not required for piRNA biogenesis, and our studies suggest that Pelo may function at the translational level to silence TEs: This function requires interaction with Hbs1, and overexpression of RpS30a partially reverts TE‐Silencing defects in pelo mutants. Interestingly, TE Silencing and spermatogenesis defects in pelo mutants can also effectively be rescued by expressing the mammalian ortholog of Pelo. We propose that the Pelo‐Hbs1 surveillance complex provides another level of defense against the expression of TEs in the germline of Drosophila and possibly all metazoa.
-
The RNA surveillance complex Pelo‐Hbs1 is required for Transposon Silencing in the Drosophila germline
EMBO reports, 2015Co-Authors: Fu Yang, Rui Zhao, Xiaofeng Fang, Huanwei Huang, Yang Xuan, Hongyan Chen, Tao CaiAbstract:Abstract Silencing of transposable elements (TEs) in the metazoan germline is critical for genome integrity and is primarily dependent on Piwi proteins and associated RNAs, which exert their function through both transcriptional and posttranscriptional mechanisms. Here, we report that the evolutionarily conserved Pelo (Dom34)‐Hbs1 mRNA surveillance complex is required for Transposon Silencing in the Drosophila germline. In pelo mutant gonads, mRNAs and proteins of some selective TEs are up‐regulated. Pelo is not required for piRNA biogenesis, and our studies suggest that Pelo may function at the translational level to silence TEs: This function requires interaction with Hbs1, and overexpression of RpS30a partially reverts TE‐Silencing defects in pelo mutants. Interestingly, TE Silencing and spermatogenesis defects in pelo mutants can also effectively be rescued by expressing the mammalian ortholog of Pelo. We propose that the Pelo‐Hbs1 surveillance complex provides another level of defense against the expression of TEs in the germline of Drosophila and possibly all metazoa.
Fu Yang - One of the best experts on this subject based on the ideXlab platform.
-
Silencing transposable elements in the Drosophila germline
Cellular and Molecular Life Sciences, 2016Co-Authors: Fu Yang, Rongwen XiAbstract:Transposable elements or Transposons are DNA pieces that can move around within the genome and are, therefore, potential threat to genome stability and faithful transmission of the genetic information in the germline. Accordingly, self-defense mechanisms have evolved in the metazoan germline to silence Transposons, and the primary mechanism requires the germline-specific non-coding small RNAs, named Piwi-interacting RNA (piRNAs), which are in complex with Argonaute family of PIWI proteins (the piRNA–RISC complexes), to silence Transposons. piRNA-mediated Transposon Silencing occurs at both transcriptional and post-transcriptional levels. With the advantages of genetic manipulation and advances of sequencing technology, much progress has been made on the molecular mechanisms of piRNA-mediated Transposon Silencing in Drosophila melanogaster, which will be the focus of this review. Because piRNA-mediated Transposon Silencing is evolutionarily conserved in metazoan, model organisms, such as Drosophila, will continue to be served as pioneer systems towards the complete understanding of Transposon Silencing in the metazoan germline.
-
the rna surveillance complex pelo hbs1 is required for Transposon Silencing in the drosophila germline
EMBO Reports, 2015Co-Authors: Fu Yang, Rui Zhao, Xiaofeng Fang, Huanwei Huang, Yang Xuan, Hongyan Chen, Tao CaiAbstract:Abstract Silencing of transposable elements (TEs) in the metazoan germline is critical for genome integrity and is primarily dependent on Piwi proteins and associated RNAs, which exert their function through both transcriptional and posttranscriptional mechanisms. Here, we report that the evolutionarily conserved Pelo (Dom34)‐Hbs1 mRNA surveillance complex is required for Transposon Silencing in the Drosophila germline. In pelo mutant gonads, mRNAs and proteins of some selective TEs are up‐regulated. Pelo is not required for piRNA biogenesis, and our studies suggest that Pelo may function at the translational level to silence TEs: This function requires interaction with Hbs1, and overexpression of RpS30a partially reverts TE‐Silencing defects in pelo mutants. Interestingly, TE Silencing and spermatogenesis defects in pelo mutants can also effectively be rescued by expressing the mammalian ortholog of Pelo. We propose that the Pelo‐Hbs1 surveillance complex provides another level of defense against the expression of TEs in the germline of Drosophila and possibly all metazoa.
-
The RNA surveillance complex Pelo‐Hbs1 is required for Transposon Silencing in the Drosophila germline
EMBO reports, 2015Co-Authors: Fu Yang, Rui Zhao, Xiaofeng Fang, Huanwei Huang, Yang Xuan, Hongyan Chen, Tao CaiAbstract:Abstract Silencing of transposable elements (TEs) in the metazoan germline is critical for genome integrity and is primarily dependent on Piwi proteins and associated RNAs, which exert their function through both transcriptional and posttranscriptional mechanisms. Here, we report that the evolutionarily conserved Pelo (Dom34)‐Hbs1 mRNA surveillance complex is required for Transposon Silencing in the Drosophila germline. In pelo mutant gonads, mRNAs and proteins of some selective TEs are up‐regulated. Pelo is not required for piRNA biogenesis, and our studies suggest that Pelo may function at the translational level to silence TEs: This function requires interaction with Hbs1, and overexpression of RpS30a partially reverts TE‐Silencing defects in pelo mutants. Interestingly, TE Silencing and spermatogenesis defects in pelo mutants can also effectively be rescued by expressing the mammalian ortholog of Pelo. We propose that the Pelo‐Hbs1 surveillance complex provides another level of defense against the expression of TEs in the germline of Drosophila and possibly all metazoa.
Gregory J. Hannon - One of the best experts on this subject based on the ideXlab platform.
-
Channel Nuclear Pore Complex subunits are required for Transposon Silencing in Drosophila.
eLife, 2021Co-Authors: Marzia Munafò, Gregory J. Hannon, Victoria R Lawless, Alessandro Passera, Serena Macmillan, Susanne Bornelöv, Irmgard U Haussmann, Matthias Soller, Benjamin CzechAbstract:The Nuclear Pore Complex (NPC) is the principal gateway between nucleus and cytoplasm that enables exchange of macromolecular cargo. Composed of multiple copies of ~30 different nucleoporins (Nups), the NPC acts as a selective portal, interacting with factors which individually license passage of specific cargo classes. Here we show that two Nups of the inner channel, Nup54 and Nup58, are essential for Transposon Silencing via the PIWI-interacting RNA (piRNA) pathway in the Drosophila ovary. In ovarian follicle cells, loss of Nup54 and Nup58 results in compromised piRNA biogenesis exclusively from the flamenco locus, whereas knockdowns of other NPC subunits have widespread consequences. This provides evidence that some nucleoporins can acquire specialised roles in tissue-specific contexts. Our findings consolidate the idea that the NPC has functions beyond simply constituting a barrier to nuclear/cytoplasmic exchange, as genomic loci subjected to strong selective pressure can exploit NPC subunits to facilitate their expression.
-
Dimerisation of the PICTS complex via LC8/Cut-up drives co-transcriptional Transposon Silencing in Drosophila.
eLife, 2021Co-Authors: Evelyn L Eastwood, Marzia Munafò, Susanne Bornelöv, Benjamin Czech, Kayla A. Jara, Vasileios Frantzis, Emma Kneuss, Elisar Barbar, Gregory J. HannonAbstract:In animal gonads, the PIWI-interacting RNA (piRNA) pathway guards genome integrity in part through the co-transcriptional gene Silencing of Transposon insertions. In Drosophila ovaries, piRNA-loaded Piwi detects nascent Transposon transcripts and instructs heterochromatin formation through the Panoramix-induced co-transcriptional Silencing (PICTS) complex, containing Panoramix, Nxf2 and Nxt1. Here, we report that the highly conserved dynein light chain LC8/Cut-up (Ctp) is an essential component of the PICTS complex. Loss of Ctp results in Transposon de-repression and a reduction in repressive chromatin marks specifically at Transposon loci. In turn, Ctp can enforce transcriptional Silencing when artificially recruited to RNA and DNA reporters. We show that Ctp drives dimerisation of the PICTS complex through its interaction with conserved motifs within Panoramix. Artificial dimerisation of Panoramix bypasses the necessity for its interaction with Ctp, demonstrating that conscription of a protein from a ubiquitous cellular machinery has fulfilled a fundamental requirement for a Transposon Silencing complex.
-
dimerisation of the picts complex via lc8 cut up drives co transcriptional Transposon Silencing in drosophila
eLife, 2021Co-Authors: Evelyn L Eastwood, Marzia Munafò, Susanne Bornelöv, Benjamin Czech, Kayla A. Jara, Vasileios Frantzis, Emma Kneuss, Elisar Barbar, Gregory J. HannonAbstract:In animal gonads, the PIWI-interacting RNA (piRNA) pathway guards genome integrity in part through the co-transcriptional gene Silencing of Transposon insertions. In Drosophila ovaries, piRNA-loaded Piwi detects nascent Transposon transcripts and instructs heterochromatin formation through the Panoramix-induced co-transcriptional Silencing (PICTS) complex, containing Panoramix, Nxf2 and Nxt1. Here, we report that the highly conserved dynein light chain LC8/Cut-up (Ctp) is an essential component of the PICTS complex. Loss of Ctp results in Transposon de-repression and a reduction in repressive chromatin marks specifically at Transposon loci. In turn, Ctp can enforce transcriptional Silencing when artificially recruited to RNA and DNA reporters. We show that Ctp drives dimerisation of the PICTS complex through its interaction with conserved motifs within Panoramix. Artificial dimerisation of Panoramix bypasses the necessity for its interaction with Ctp, demonstrating that conscription of a protein from a ubiquitous cellular machinery has fulfilled a fundamental requirement for a Transposon Silencing complex.
-
Dual functions of Macpiwi1 in Transposon Silencing and stem cell maintenance in the flatworm Macrostomum lignano
RNA (New York N.Y.), 2015Co-Authors: Xin Zhou, Giorgia Battistoni, Osama El Demerdash, James Gurtowski, Julia Wunderer, Ilaria Falciatori, Peter Ladurner, Michael C. Schatz, Gregory J. Hannon, Kaja A. WasikAbstract:PIWI proteins and piRNA pathways are essential for Transposon Silencing and some aspects of gene regulation during animal germline development. In contrast to most animal species, some flatworms also express PIWIs and piRNAs in somatic stem cells, where they are required for tissue renewal and regeneration. Here, we have identified and characterized piRNAs and PIWI proteins in the emerging model flatworm Macrostomum lignano. We found that M. lignano encodes at least three PIWI proteins. One of these, Macpiwi1, acts as a key component of the canonical piRNA pathway in the germline and in somatic stem cells. Knockdown of Macpiwi1 dramatically reduces piRNA levels, derepresses Transposons, and severely impacts stem cell maintenance. Knockdown of the piRNA biogenesis factor Macvasa caused an even greater reduction in piRNA levels with a corresponding increase in Transposons. Yet, in Macvasa knockdown animals, we detected no major impact on stem cell self-renewal. These results may suggest stem cell maintenance functions of PIWI proteins in flatworms that are distinguishable from their impact on Transposons and that might function independently of what are considered canonical piRNA populations.
-
pitfalls of mapping high throughput sequencing data to repetitive sequences piwi s genomic targets still not identified
Developmental Cell, 2015Co-Authors: Georgi K Marinov, Gregory J. Hannon, Zhiping Weng, Jie Wang, Phillip D. Zamore, Dominik Handler, Barbara J Wold, Alexei A Aravin, Julius Brennecke, Katalin Fejes TothAbstract:Huang et al. (2013) recently reported that chromatin immunoprecipitation sequencing (ChIP-seq) reveals the genome-wide sites of occupancy by Piwi, a piRNA-guided Argonaute protein central to Transposon Silencing in Drosophila. Their study also reported that loss of Piwi causes widespread rewiring of transcriptional patterns, as evidenced by changes in RNA polymerase II occupancy across the genome. Here we reanalyze their data and report that the underlying deep-sequencing dataset does not support the authors' genome-wide conclusions.
Ronald H.a. Plasterk - One of the best experts on this subject based on the ideXlab platform.
-
RDE-2 interacts with MUT-7 to mediate RNA interference in Caenorhabditis elegans
Nucleic acids research, 2005Co-Authors: Bastiaan B. J. Tops, Femke Simmer, Titia Sijen, Ronald H.a. Plasterk, Hiroaki Tabara, Craig C Mello, René F. KettingAbstract:In Caenorhabditis elegans, the activity of transposable elements is repressed in the germline. One of the mechanisms involved in this repression is RNA interference (RNAi), a process in which dsRNA targets cleavage of mRNAs in a sequence-specific manner. The first gene found to be involved in RNAi and Transposon Silencing in C.elegans is mut-7, a gene encoding a putative exoribonuclease. Here, we show that the MUT-7 protein resides in complexes of � 250 kDa in the nucleus and in the cytosol. In addition, we find that upon triggering of RNAi the cytosolic MUT-7 complex increases in size. This increase is independent of the presence of target RNA, but does depend on the presence of RDE-1 and RDE-4, two proteins involved in small interfering RNA (siRNA) production. Finally, using a yeast two-hybrid screen, we identified RDE-2/ MUT-8 as one of the other components of this complex. This protein is encoded by the rde-2/mut-8 locus, previously implicated in RNAi and Transposon Silencing. Using genetic complementation analysis, we show that the interaction between these two proteins is required for efficient RNAi in vivo. Together these data support a role for the MUT-7/RDE-2 complex downstream of siRNA formation, but upstream of siRNA mediated target RNA recognition, possibly indicating a role in the siRNA amplification step.
-
RNAi protects the Caenorhabditis elegans germline against transposition.
Trends in genetics : TIG, 2004Co-Authors: Nadine L. Vastenhouw, Ronald H.a. PlasterkAbstract:The availability of complete genome sequences has revealed that genomes contain numerous mobile genetic elements. The activity of these Transposons results in genome instability. In the nematode Caenorhabditis elegans, transposition is silenced in the germline, protecting the genome from heritable defects that are caused by Transposon jumps. The discovery of RNA interference (RNAi) has greatly increased our understanding of this genome-defense mechanism because Transposon Silencing and RNAi share common factors. RNAi is the post-transcriptional Silencing of a gene in response to double-stranded RNA (dsRNA), which is processed into small interfering RNAs (siRNAs) that mediate sequence-specific RNA degradation. Indeed, Transposon-derived dsRNA and siRNAs are detected in vivo and are capable of inducing Silencing. In addition, many new genes have been identified that are required for the Silencing of Transposons. In this article, we discuss our current model for Transposon Silencing and address several unanswered questions because many aspects of this protection mechanism in C. elegans might be present in a broad range of organisms.
-
Transposon Silencing in the caenorhabditis elegans germ line by natural rnai
Nature, 2003Co-Authors: Titia Sijen, Ronald H.a. PlasterkAbstract:Transposable elements are stretches of DNA that can move and multiply within the genome of an organism. The Caenorhabditis elegans genome contains multiple Tc1 Transposons that jump in somatic cells, but are silenced in the germ line1,2,3. Many mutants that have lost this Silencing have also lost the ability to execute RNA interference (RNAi)2,3, a process whereby genes are suppressed by exposure to homologous double-stranded RNA (dsRNA). Here we show how RNAi causes Transposon Silencing in the nematode germ line. We find evidence for Transposon-derived dsRNAs, in particular to the terminal inverted repeats, and show that these RNAs may derive from read-through transcription of entire transposable elements. Small interfering RNAs of Tc1 were detected. When a germline-expressed reporter gene is fused to a stretch of Tc1 sequence, this transgene is silenced in a manner dependent on functional mutator genes (mut-7, mut-16 and pk732). These results indicate that RNAi surveillance is triggered by fortuitous read-through transcription of dispersed Tc1 copies, which can form dsRNA as a result of ‘snap-back’ of the terminal inverted repeats. RNAi mediated by this dsRNA silences transposase gene expression.
-
A Genome-Wide Screen Identifies 27 Genes Involved in Transposon Silencing in C. elegans
Current biology : CB, 2003Co-Authors: Nadine L. Vastenhouw, Sylvia E. J. Fischer, Valérie J.p. Robert, Karen L. Thijssen, Andrew G. Fraser, Ravi S. Kamath, Julie Ahringer, Ronald H.a. PlasterkAbstract:Transposon jumps are a major cause of genome instability. In the C. elegans strain Bristol N2, Transposons are active in somatic cells, but they are silenced in the germline [1], presumably to protect the germline from mutations. Interestingly, the Transposon-Silencing mechanism shares factors with the RNAi machinery [2]. To better understand the mechanism of Transposon Silencing, we performed a genome-wide RNAi screen for genes that, when silenced, cause transposition of Tc1 in the C. elegans germline. We identified 27 such genes, among which are mut-16, a mutator that was previously found but not identified at the molecular level, ppw-2, a member of the argonaute family, and several factors that indicate a role for chromatin structure in the regulation of transposition. Some of the newly identified genes are also required for cosuppression and therefore represent the shared components of the two pathways. Since most of the newly identified genes have clear homologs in other species, and since Transposons are found from protozoa to human, it seems likely that they also protect other genomes against Transposon activity in the germline.
-
The Mechanism of RNA Interference and the Transposon Silencing in Caenorhabditis elegans.
TheScientificWorldJournal, 2002Co-Authors: Marcel Tijsterman, Rena Ketting, Sylvia E. J. Fischer, Femke Simmer, Titia Sijen, Kristy L. Okihara, Bas Tops, Nadine L. Vastenhouw, Ronald H.a. PlasterkAbstract:INTRODUCTION. All isolates of C. elegans contain multiple transposable elements in their genome. These elements jump around freely in somatic cells, but transposition is fully silenced in the germline. In investigating the mechanism of Transposon Silencing, we found that it was mechanistically linked to another phenomenon: RNAi or RNA interference. This is the experimental Silencing of gene expression by administration of double-stranded RNA.
