RNA Helicase MUT-14-Dependent Gene Silencing Triggered in C. elegans by Short Antisense RNAs

Science ◽  
2002 ◽  
Vol 295 (5555) ◽  
pp. 694-697 ◽  
Author(s):  
M. Tijsterman
Keyword(s):  
Gene Silencing ◽  
Rna Helicase ◽  
Antisense Rnas ◽  
C Elegans

scholarly journals Intronic MicroRNA (miRNA)

2006 ◽  
Vol 2006 ◽  
pp. 1-13 ◽  
Author(s):  
Shi-Lung Lin ◽  
Joseph D. Miller ◽  
Shao-Yao Ying
Keyword(s):  
Rna Interference ◽  
Gene Silencing ◽  
Regulatory System ◽  
Fine Tuning ◽  
Messenger Rnas ◽  
Noncoding Dna ◽  
Protein Coding ◽  
C Elegans ◽  
Adult Mice

Nearly 97% of the human genome is composed of noncoding DNA, which varies from one species to another. Changes in these sequences often manifest themselves in clinical and circumstantial malfunction. Numerous genes in these non-protein-coding regions encode microRNAs, which are responsible for RNA-mediated gene silencing through RNA interference (RNAi)-like pathways. MicroRNAs (miRNAs), small single-stranded regulatory RNAs capable of interfering with intracellular messenger RNAs (mRNAs) with complete or partial complementarity, are useful for the design of new therapies against cancer polymorphisms and viral mutations. Currently, many varieties of miRNA are widely reported in plants, animals, and even microbes. Intron-derived microRNA (Id-miRNA) is a new class of miRNA derived from the processing of gene introns. The intronic miRNA requires type-II RNA polymerases (Pol-II) and spliceosomal components for their biogenesis. Several kinds of Id-miRNA have been identified inC elegans, mouse, and human cells; however, neither function nor application has been reported. Here, we show for the first time that intron-derived miRNAs are able to induce RNA interference in not only human and mouse cells, but in also zebrafish, chicken embryos, and adult mice, demonstrating the evolutionary preservation of intron-mediated gene silencing via functional miRNA in cell and in vivo. These findings suggest an intracellular miRNA-mediated gene regulatory system, fine-tuning the degradation of protein-coding messenger RNAs.

scholarly journals The DEAD Box RNA Helicase VBH-1 Is a New Player in the Stress Response in C. elegans

PLoS ONE ◽  
2014 ◽  
Vol 9 (5) ◽  
pp. e97924 ◽  
Author(s):  
Daniel Paz-Gómez ◽  
Emmanuel Villanueva-Chimal ◽  
Rosa E. Navarro
Keyword(s):  
Stress Response ◽  
Rna Helicase ◽  
C Elegans ◽  
Dead Box ◽  
The Dead

scholarly journals RNA helicase A is important for germline transcriptional control, proliferation, and meiosis in C. elegans

2005 ◽  
Vol 122 (5) ◽  
pp. 707-720 ◽  
Author(s):  
Katherine M. Walstrom ◽  
Deborah Schmidt ◽  
Christopher J. Bean ◽  
William G. Kelly
Keyword(s):  
Transcriptional Control ◽  
Rna Helicase ◽  
Rna Helicase A ◽  
C Elegans

scholarly journals poly(UG)-tailed RNAs in Genome Protection and Epigenetic Inheritance

2019 ◽  
Author(s):  
Aditi Shukla ◽  
Jenny Yan ◽  
Daniel J. Pagano ◽  
Anne E. Dodson ◽  
Yuhan Fei ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Epigenetic Inheritance ◽  
Genome Integrity ◽  
Small Interfering Rnas ◽  
Genetic Elements ◽  
C Elegans ◽  
Transposon Silencing ◽  
Rna Fragments ◽  
Heterologous Expression Systems ◽  
Genome Protection

AbstractMobile genetic elements threaten genome integrity in all organisms. MUT-2/RDE-3 is a ribonucleotidyltransferase required for transposon silencing and RNA interference (RNAi) in C. elegans. When tethered to RNAs in heterologous expression systems, RDE-3 can add long stretches of alternating non-templated uridine (U) and guanosine (G) ribonucleotides to the 3’ termini of these RNAs (polyUG or pUG tails). Here, we show that, in its natural context in C. elegans, RDE-3 adds pUG tails to transposon RNAs, as well as to targets of RNAi. pUG tails with more than 16 perfectly alternating 3’ U and G nucleotides convert otherwise inert RNA fragments into agents of gene silencing. pUG tails promote gene silencing by recruiting RNA-dependent RNA Polymerases (RdRPs), which use pUG-tailed RNAs as templates to synthesize small interfering RNAs (siRNAs). Cycles of pUG RNA-templated siRNA synthesis and siRNA-directed mRNA pUGylation underlie dsRNA-directed transgenerational epigenetic inheritance in the C. elegans germline. Our results show that pUG tails convert RNAs into transgenerational memories of past gene silencing events, which, we speculate, allow parents to inoculate progeny against the expression of unwanted or parasitic genetic elements.

scholarly journals A genome-wide screening for RNAi pathway proteins in Acari

2020 ◽  
Author(s):  
Beatrice T Nganso ◽  
Noa Sela ◽  
Victoria Soroker
Keyword(s):  
Gene Silencing ◽  
Micro Rna ◽  
Rnai Pathway ◽  
Comparative Genomic ◽  
Specific Gene ◽  
C Elegans ◽  
Conserved Sequence ◽  
A Genome ◽  
Systemic Rnai ◽  
Amplification Mechanism

Abstract Background RNA interference (RNAi) is a highly conserved, sequence-specific gene silencing mechanism present in Eukaryotes. Three RNAi pathways critical for organismal development and survival are known, namely micro-RNA (miRNA), Piwi-interacting RNA (piRNA) and short interfering RNA (siRNA) pathways. Little knowledge exist about the genes involved in these pathways in Acari. Moreover, variable successes has been obtained in gene knockdown via siRNA pathway in functional genomics and management of Acari species. We hypothesized that the clue may be in the variability in the composition and the efficacy of siRNAi machinery among Acari. Results Both comparative genomic analyses and domain annotation suggest that all the analyzed species have orthologs of genes that mediate gene silencing via the three RNAi pathways though gene duplication and/or loss have occurred in the different species. We also identified orthologs of Caenorhabditis elegans RNA-dependent RNA polymerase (RdRP) gene in all Acari species though no secondary Argonaute homologs that operate with this gene in siRNA amplification mechanism were found. This finding suggests that the siRNA amplification mechanism present in Acari may be distinct from that described in C. elegans . Moreover, the genomes of these Acari species encode no ortholog of C. elegans systemic RNAi defective 1 (Sid-1) that mediate systemic RNAi, suggesting that the phenomena of systemic and parental RNAi that has been reported in some Acari species probably occur through a different mechanism. Orthologs of RNAi spreading defective-3 (Rsd-3) gene and scavenger receptors namely Eater and SR-CI that mediate endocytosis cellular update of dsRNA in C. elegans and Drosophila melanogaster were found in Acari genomes. This result suggests that cellular dsRNA uptake in Acari is endocytosis-dependent. Detailed phylogenetic analyses of core RNAi pathway genes in the studied Acari species revealed that their evolution is compatible with the proposed monophyletic evolution of this group. Conclusions Taken together, our in silico comparative analyses have revealed the potential activity of all three pathways in Acari. However, much experimental work remains to be done in elucidating the operating mechanisms behind these pathways in particular those that govern systemic/parental RNAi and siRNA amplification in Acari.

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