scholarly journals Kcnq1ot1 noncoding RNA mediates transcriptional gene silencing by interacting with Dnmt1

Development ◽  
2010 ◽  
Vol 137 (15) ◽  
pp. 2493-2499 ◽  
Author(s):  
F. Mohammad ◽  
T. Mondal ◽  
N. Guseva ◽  
G. K. Pandey ◽  
C. Kanduri
Keyword(s):  
Gene Silencing ◽  
Noncoding Rna ◽  
Transcriptional Gene Silencing

Long noncoding RNA-mediated maintenance of DNA methylation and transcriptional gene silencing

2012 ◽  
Vol 125 (15) ◽  
pp. e1-e1
Author(s):  
F. Mohammad ◽  
G. K. Pandey ◽  
T. Mondal ◽  
S. Enroth ◽  
L. Redrup ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Silencing ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Transcriptional Gene Silencing

scholarly journals Long noncoding RNA-mediated intrachromosomal interactions promote imprinting at the Kcnq1 locus

2014 ◽  
Vol 204 (1) ◽  
pp. 61-75 ◽  
Author(s):  
He Zhang ◽  
Michael J. Zeitz ◽  
Hong Wang ◽  
Beibei Niu ◽  
Shengfang Ge ◽  
...  
Keyword(s):  
Gene Silencing ◽  
Long Range ◽  
Ribonucleic Acid ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Transcriptional Gene Silencing ◽  
Chromatin Conformation ◽  
Polycomb Repressive Complex 2 ◽  
Allele Specific ◽  
Capture Method

Kcnq1ot1 is a long noncoding ribonucleic acid (RNA; lncRNA) that participates in the regulation of genes within the Kcnq1 imprinting domain. Using a novel RNA-guided chromatin conformation capture method, we demonstrate that the 5′ region of Kcnq1ot1 RNA orchestrates a long-range intrachromosomal loop between KvDMR1 and the Kcnq1 promoter that is required for maintenance of imprinting. PRC2 (polycomb repressive complex 2), which participates in the allelic repression of Kcnq1, is also recruited by Kcnq1ot1 RNA via EZH2. Targeted suppression of Kcnq1ot1 lncRNA prevents the creation of this long-range intrachromosomal loop and causes loss of Kcnq1 imprinting. These observations delineate a novel mechanism by which an lncRNA directly builds an intrachromosomal interaction complex to establish allele-specific transcriptional gene silencing over a large chromosomal domain.

scholarly journals Long noncoding RNA-mediated maintenance of DNA methylation and transcriptional gene silencing

Development ◽  
2012 ◽  
Vol 139 (15) ◽  
pp. 2792-2803 ◽  
Author(s):  
F. Mohammad ◽  
G. K. Pandey ◽  
T. Mondal ◽  
S. Enroth ◽  
L. Redrup ◽  
...  
Keyword(s):  
Dna Methylation ◽  
Gene Silencing ◽  
Long Noncoding Rna ◽  
Noncoding Rna ◽  
Transcriptional Gene Silencing

scholarly journals Viroids as a Tool to Study RNA-Directed DNA Methylation in Plants

Cells ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 1187
Author(s):  
Michael Wassenegger ◽  
Athanasios Dalakouras
Keyword(s):  
Dna Methylation ◽  
Rna Interference ◽  
Gene Silencing ◽  
Plant Cells ◽  
Transcriptional Gene Silencing ◽  
Rnai Machinery ◽  
Double Stranded Rna ◽  
Post Transcriptional Gene Silencing ◽  
Cumulative Amount

Viroids are plant pathogenic, circular, non-coding, single-stranded RNAs (ssRNAs). Members of the Pospiviroidae family replicate in the nucleus of plant cells through double-stranded RNA (dsRNA) intermediates, thus triggering the host’s RNA interference (RNAi) machinery. In plants, the two RNAi pillars are Post-Transcriptional Gene Silencing (PTGS) and RNA-directed DNA Methylation (RdDM), and the latter has the potential to trigger Transcriptional Gene Silencing (TGS). Over the last three decades, the employment of viroid-based systems has immensely contributed to our understanding of both of these RNAi facets. In this review, we highlight the role of Pospiviroidae in the discovery of RdDM, expound the gradual elucidation through the years of the diverse array of RdDM’s mechanistic details and propose a revised RdDM model based on the cumulative amount of evidence from viroid and non-viroid systems.

scholarly journals Epigenetic Changes in Host Ribosomal DNA Promoter Induced by an Asymptomatic Plant Virus Infection

Biology ◽  
2020 ◽  
Vol 9 (5) ◽  
pp. 91 ◽  
Author(s):  
Miryam Pérez-Cañamás ◽  
Elizabeth Hevia ◽  
Carmen Hernández
Keyword(s):  
Gene Silencing ◽  
Ribosomal Dna ◽  
Plant Virus ◽  
Dna Methyltransferase ◽  
Cytosine Methylation ◽  
De Novo ◽  
Methylation Pattern ◽  
Transcriptional Gene Silencing ◽  
Post Transcriptional Gene Silencing ◽  
The Impact

DNA cytosine methylation is one of the main epigenetic mechanisms in higher eukaryotes and is considered to play a key role in transcriptional gene silencing. In plants, cytosine methylation can occur in all sequence contexts (CG, CHG, and CHH), and its levels are controlled by multiple pathways, including de novo methylation, maintenance methylation, and demethylation. Modulation of DNA methylation represents a potentially robust mechanism to adjust gene expression following exposure to different stresses. However, the potential involvement of epigenetics in plant-virus interactions has been scarcely explored, especially with regard to RNA viruses. Here, we studied the impact of a symptomless viral infection on the epigenetic status of the host genome. We focused our attention on the interaction between Nicotiana benthamiana and Pelargonium line pattern virus (PLPV, family Tombusviridae), and analyzed cytosine methylation in the repetitive genomic element corresponding to ribosomal DNA (rDNA). Through a combination of bisulfite sequencing and RT-qPCR, we obtained data showing that PLPV infection gives rise to a reduction in methylation at CG sites of the rDNA promoter. Such a reduction correlated with an increase and decrease, respectively, in the expression levels of some key demethylases and of MET1, the DNA methyltransferase responsible for the maintenance of CG methylation. Hypomethylation of rDNA promoter was associated with a five-fold augmentation of rRNA precursor levels. The PLPV protein p37, reported as a suppressor of post-transcriptional gene silencing, did not lead to the same effects when expressed alone and, thus, it is unlikely to act as suppressor of transcriptional gene silencing. Collectively, the results suggest that PLPV infection as a whole is able to modulate host transcriptional activity through changes in the cytosine methylation pattern arising from misregulation of methyltransferases/demethylases balance.

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