scholarly journals Genome-wide identification of long non-coding RNA targets of the tomato MADS box transcription factor RIN and function analysis

2018 ◽  
Vol 123 (3) ◽  
pp. 469-482 ◽  
Author(s):  
Tongtong Yu ◽  
David T W Tzeng ◽  
Ran Li ◽  
Jianye Chen ◽  
Silin Zhong ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Function Analysis ◽  
Mads Box ◽  
Non Coding Rna ◽  
Rna Targets ◽  
Genome Wide ◽  
And Function ◽  
Long Non Coding Rna

scholarly journals ciRS-7 exonic sequence is embedded in a long non-coding RNA locus

2017 ◽  
Author(s):  
Steven P. Barrett ◽  
Kevin R. Parker ◽  
Caroline Horn ◽  
Miguel Mata ◽  
Julia Salzman
Keyword(s):  
Circular Rnas ◽  
Biological Regulation ◽  
Functional Roles ◽  
Rna Transcripts ◽  
Non Coding Rna ◽  
Genome Wide ◽  
And Function ◽  
Long Non Coding Rna ◽  
Human And Mouse ◽  
Exonic Sequence

AbstractciRS-7 is an intensely studied, highly expressed and conserved circRNA. Essentially nothing is known about its biogenesis, including the location of its promoter. A prevailing assumption has been that ciRS-7 is an exceptional circRNA because it is transcribed from a locus lacking any mature linear RNA transcripts of the same sense. Our interest in the biogenesis of ciRS-7 led us to develop an algorithm to define its promoter. This approach predicted that the human ciRS-7 promoter coincides with that of the long non-coding RNA, LINC00632. We validated this prediction using multiple orthogonal experimental assays. We also used computational approaches and experimental validation to establish that ciRS-7 exonic sequence is embedded in linear transcripts that are flanked by cryptic exons in both human and mouse. Together, this experimental and computational evidence generate a new view of regulation in this locus: (a) ciRS-7 is like other circRNAs, as it is spliced into linear transcripts; (b) expression of ciRS-7 is primarily determined by the chromatin state of LINC00632 promoters; (c) transcription and splicing factors sufficient for ciRS-7 biogenesis are expressed in cells that lack detectable ciRS-7 expression. These findings have significant implications for the study of the regulation and function of ciRS-7, and the analytic framework we developed to jointly analyze RNA-seq and ChlP-seq data reveal the potential for genome-wide discovery of important biological regulation missed in current reference annotations.Author SummarycircRNAs were recently discovered to be a significant product of ‘host’ gene expression programs but little is known about their transcriptional regulation. Here, we have studied the expression of a well-known circRNA named ciRS-7. ciRS-7 has an unusual function for a circRNA; it is believed to be a miRNA sponge. Previously, ciRS-7 was thought to be transcribed from a locus lacking any mature linear isoforms, unlike all other circular RNAs known to be expressed in human cells. However, we have found this to be false; using a combination of bioinformatic and experimental genetic approaches, in both human and mouse, we discovered that linear transcripts containing the ciRS-7 exonic sequence, linking it to upstream genes. This suggests the potential for additional functional roles of this important locus and provides critical information to begin study on the biogenesis of ciRS-7.

scholarly journals The PVT1 lncRNA is a novel epigenetic enhancer of MYC, and a promising risk-stratification biomarker in colorectal cancer

2020 ◽  
Vol 19 (1) ◽  
Author(s):  
Kunitoshi Shigeyasu ◽  
Shusuke Toden ◽  
Tsuyoshi Ozawa ◽  
Takatoshi Matsuyama ◽  
Takeshi Nagasaka ◽  
...  
Keyword(s):  
Colorectal Cancer ◽  
Aberrant Methylation ◽  
Enhancer Activity ◽  
Transcriptional Enhancers ◽  
Cancer Pathogenesis ◽  
Non Coding Rna ◽  
Genome Wide ◽  
A Genome ◽  
And Function ◽  
Long Non Coding Rna

Abstract Accumulating evidence suggests that dysregulation of transcriptional enhancers plays a significant role in cancer pathogenesis. Herein, we performed a genome-wide discovery of enhancer elements in colorectal cancer (CRC). We identified PVT1 locus as a previously unrecognized transcriptional regulator in CRC with a significantly high enhancer activity, which ultimately was responsible for regulating the expression of MYC oncogene. High expression of the PVT1 long-non-coding RNA (lncRNA) transcribed from the PVT1 locus was associated with poor survival among patients with stage II and III CRCs (p < 0.05). Aberrant methylation of the PVT1 locus inversely correlated with the reduced expression of the corresponding the PVT1 lncRNA, as well as MYC gene expression. Bioinformatic analyses of CRC-transcriptomes revealed that the PVT1 locus may also broadly impact the expression and function of other key genes within two key CRC-associated signaling pathways – the TGFβ/SMAD and Wnt/β-Catenin pathways. We conclude that the PVT1 is a novel oncogenic enhancer of MYC and its activity is controlled through epigenetic regulation mediated through aberrant methylation in CRC. Our findings also suggest that the PVT1 lncRNA expression is a promising prognostic biomarker and a potential therapeutic target in CRC.

scholarly journals Sox2-Evf2 lncRNA mechanisms of chromosome topological control in developing forebrain

Development ◽  
2021 ◽  
pp. dev.197202
Author(s):  
Ivelisse Cajigas ◽  
Abhijit Chakraborty ◽  
Madison Lynam ◽  
Kelsey R. Swyter ◽  
Monique Bastidas ◽  
...  
Keyword(s):  
Transcription Factor ◽  
Dna Binding ◽  
Long Range ◽  
Target Gene ◽  
Gene Repression ◽  
Ribonucleoprotein Complex ◽  
Interaction Sites ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Long Non Coding Rna

The Evf2 long non-coding RNA directs Dlx5/6 ultraconserved enhancer(UCE)-intrachromosomal interactions, regulating genes across a 27Mb region on chr6 in mouse developing forebrain. Here, we show that Evf2 long-range gene repression occurs through multi-step mechanisms involving the transcription factor Sox2. Evf2 directly interacts with Sox2, antagonizing Sox2 activation of Dlx5/6UCE, and recruits Sox2 to the Dlx5/6eii shadow enhancer and key Dlx5/6UCE interaction sites. Sox2 directly interacts with Dlx1 and Smarca4, as part of the Evf2 ribonucleoprotein complex, forming spherical subnuclear domains (protein pools, PPs). Evf2 targets Sox2 PPs to one long-range repressed target gene (Rbm28), at the expense of another (Akr1b8).Evf2 and Sox2 shift Dlx5/6UCE interactions towards Rbm28, linking Evf2/Sox2 co-regulated topological control and gene repression. We propose a model that distinguishes Evf2 gene repression mechanisms at Rbm28 (Dlx5/6UCE position) and Akr1b8 (limited Sox2 availability). Genome-wide control of RNPs (Sox2, Dlx and Smarca4) shows that co-recruitment influences Sox2 DNA binding. Together, these data suggest that Evf2 organizes a Sox2 PP subnuclear domain, and through Sox2-RNP sequestration and recruitment, regulates chr6 long-range UCE targeting and activity with genome-wide consequences.

scholarly journals Pharmacogenomics of Lithium Response in Bipolar Disorder

2021 ◽  
Vol 14 (4) ◽  
pp. 287
Author(s):  
Courtney M. Vecera ◽  
Gabriel R. Fries ◽  
Lokesh R. Shahani ◽  
Jair C. Soares ◽  
Rodrigo Machado-Vieira
Keyword(s):  
Bipolar Disorder ◽  
Association Studies ◽  
Mood Stabilizer ◽  
Genome Wide Association Studies ◽  
Nucleotide Polymorphisms ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Lithium Response ◽  
Genetic Loading ◽  
Long Non Coding Rna

Despite being the most widely studied mood stabilizer, researchers have not confirmed a mechanism for lithium’s therapeutic efficacy in Bipolar Disorder (BD). Pharmacogenomic applications may be clinically useful in the future for identifying lithium-responsive patients and facilitating personalized treatment. Six genome-wide association studies (GWAS) reviewed here present evidence of genetic variations related to lithium responsivity and side effect expression. Variants were found on genes regulating the glutamate system, including GAD-like gene 1 (GADL1) and GRIA2 gene, a mutually-regulated target of lithium. In addition, single nucleotide polymorphisms (SNPs) discovered on SESTD1 may account for lithium’s exceptional ability to permeate cell membranes and mediate autoimmune and renal effects. Studies also corroborated the importance of epigenetics and stress regulation on lithium response, finding variants on long, non-coding RNA genes and associations between response and genetic loading for psychiatric comorbidities. Overall, the precision medicine model of stratifying patients based on phenotype seems to derive genotypic support of a separate clinical subtype of lithium-responsive BD. Results have yet to be expounded upon and should therefore be interpreted with caution.

scholarly journals Functional genomics of autoimmune diseases

2021 ◽  
pp. annrheumdis-2019-216794
Author(s):  
Akari Suzuki ◽  
Matteo Maurizio Guerrini ◽  
Kazuhiko Yamamoto
Keyword(s):  
Autoimmune Diseases ◽  
Association Studies ◽  
Linkage Disequilibrium Block ◽  
Causal Variant ◽  
Genome Wide Association Studies ◽  
Coding Region ◽  
Risk Variants ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Long Non Coding Rna

For more than a decade, genome-wide association studies have been applied to autoimmune diseases and have expanded our understanding on the pathogeneses. Genetic risk factors associated with diseases and traits are essentially causative. However, elucidation of the biological mechanism of disease from genetic factors is challenging. In fact, it is difficult to identify the causal variant among multiple variants located on the same haplotype or linkage disequilibrium block and thus the responsible biological genes remain elusive. Recently, multiple studies have revealed that the majority of risk variants locate in the non-coding region of the genome and they are the most likely to regulate gene expression such as quantitative trait loci. Enhancer, promoter and long non-coding RNA appear to be the main target mechanisms of the risk variants. In this review, we discuss functional genetics to challenge these puzzles.

Genome-wide identification and expression analysis of the MADS-box transcription factor family in Camellia sinensis

2021 ◽  
Vol 62 (2) ◽  
pp. 249-264
Author(s):  
Zai-Bao Zhang ◽  
Yuan-Jin Jin ◽  
Hou-Hong Wan ◽  
Lin Cheng ◽  
Zhi-Guo Feng
Keyword(s):  
Transcription Factor ◽  
Expression Analysis ◽  
Camellia Sinensis ◽  
Mads Box ◽  
Transcription Factor Family ◽  
Genome Wide

Genome-wide analysis of long non-coding RNA expression profiles in keratinocytes from psoriasis skin

2021 ◽  
Author(s):  
Longlong Luo ◽  
Nupur khera ◽  
Andor Pivarcsi ◽  
Ankit Srivastava ◽  
Lorenzo Pasquali ◽  
...  
Keyword(s):  
Expression Profiles ◽  
Rna Expression ◽  
Genome Wide Analysis ◽  
Non Coding Rna ◽  
Genome Wide ◽  
Long Non Coding Rna

scholarly journals TUG1 promotes prostate cancer progression by acting as a ceRNA of miR-26a

2018 ◽  
Vol 38 (5) ◽  
Author(s):  
Bin Yang ◽  
Xiaodi Tang ◽  
Zhixin Wang ◽  
Daju Sun ◽  
Xin Wei ◽  
...  
Keyword(s):  
Prostate Cancer ◽  
Cancer Progression ◽  
Migration And Invasion ◽  
Tumor Cell Migration ◽  
Real Time Quantitative Pcr ◽  
Non Coding Rna ◽  
Key Aspects ◽  
And Function ◽  
First Time ◽  
Long Non Coding Rna

Previous studies have demonstrated that taurine-upregulated gene 1 (TUG1) was aberrantly expressed and involved in multiple types of cancer; however, the expression profile and potential role of TUG1 in prostate cancer (PCa) remains unclear. The aim of the present study was to evaluate the expression and function of TUG1 in PCa. In the present study, we analyzed TUG1 expression levels of PCa patients in tumor and adjacent normal tissue by real-time quantitative PCR. Knockdown of TUG1 by RNAi was performed to explore its roles in cell proliferation, migration, and invasion. Here we report, for the first time, that TUG1 promotes tumor cell migration, invasion, and proliferation in PCa by working in key aspects of biological behaviors. TUG1 could negatively regulate the expression of miR-26a in PCa cells. The bioinformatics prediction revealed putative miR-26a-binding sites within TUG1 transcripts. In conclusion, our study suggests that long non-coding RNA (lncRNA) TUG1 acts as a functional oncogene in PCa development.

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