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2022 ◽  
Vol 11 ◽  
Author(s):  
Soudeh Ghafouri-Fard ◽  
Tayyebeh Khoshbakht ◽  
Mohammad Taheri ◽  
Seyedpouzhia Shojaei

Sprouty RTK signaling antagonist 4-intronic transcript 1 (SPRY4-IT1) is a long non-coding RNA (lncRNA) encoded by a gene located on 5q31.3. This lncRNA has a possible role in the regulation of cell growth, proliferation, and apoptosis. Moreover, since SPRY4-IT1 controls levels of lipin 2, it is also involved in the biosynthesis of lipids. During the process of biogenesis, SPRY4-IT1 is produced as a primary transcript which is then cleaved to generate a mature transcript which is localized in the cytoplasm. SPRY4-IT1 has oncogenic roles in diverse tissues. A possible route of participation of SPRY4-IT1 in the carcinogenesis is through sequestering miRNAs such as miR-101-3p, miR‐6882‐3p and miR-22-3p. The sponging effect of SPRY4-IT1 on miR-101 has been verified in colorectal cancer, osteosarcoma, cervical cancer, bladder cancer, gastric cancer and cholangiocarcinoma. SPRY4-IT1 has functional interactions with HIF-1α, NF-κB/p65, AMPK, ZEB1, MAPK and PI3K/Akt signaling. We explain the role of SPRY4-IT1 in the carcinogenesis according to evidence obtained from cell lines, xenograft models and clinical studies.


Author(s):  
Xiao Li ◽  
Janice M Zengel ◽  
Lasse Lindahl

Processing of the RNA polymerase I pre-rRNA transcript into the mature 18S, 5.8S, and 25S rRNAs requires removing the “spacer” sequences. The canonical pathway for the removal of the ITS1 spacer, located between 18S and 5.8S rRNAs in the primary transcript, involves cleavages at the 3’ end of 18S rRNA and at two sites inside ITS1. The process generates a long and a short 5.8S rRNA that differ in the number of ITS1 nucleotides retained at the 5.8S 5’ end. Here we document a novel pathway that generates the long 5.8S for ITS1 while bypassing cleavage within ITS1. It entails a single endonuclease cut at the 3’-end of 18S rRNA followed by exonuclease Xrn1 degradation of ITS1. Mutations in RNase MRP increase the accumulation of long relative to short 5.8S rRNA; traditionally this is attributed to a decreased rate of RNase MRP cleavage at its target in ITS1, called A3. In contrast, we report here that the MRP induced switch between long and short 5.8S rRNA formation occurs even when the A3 site is deleted. Based on this and our published data, we propose that the switch may depend on RNase MRP processing RNA molecules other than pre-rRNA.


2021 ◽  
Vol 8 ◽  
Author(s):  
Sarbottam Piya ◽  
Valeria S. Lopes-Caitar ◽  
Won‐Seok Kim ◽  
Vince Pantalone ◽  
Hari B. Krishnan ◽  
...  

DNA methylation has recently emerged as a powerful regulatory mechanism controlling the expression of key regulators of various developmental processes, including nodulation. However, the functional role of DNA methylation in regulating the expression of microRNA (miRNA) genes during the formation and development of nitrogen-fixing nodules remains largely unknown. In this study, we profiled DNA methylation patterns of miRNA genes during nodule formation, development, and early senescence stages in soybean (Glycine max) through the analysis of methylC—seq data. Absolute DNA methylation levels in the CG, CHH, and CHH sequence contexts over the promoter and primary transcript regions of miRNA genes were significantly higher in the nodules compared with the corresponding root tissues at these three distinct nodule developmental stages. We identified a total of 82 differentially methylated miRNAs in the nodules compared with roots. Differential DNA methylation of these 82 miRNAs was detected only in the promoter (69), primary transcript region (3), and both in the promoter and primary transcript regions (10). The large majority of these differentially methylated miRNAs were hypermethylated in nodules compared with the corresponding root tissues and were found mainly in the CHH context and showed stage-specific methylation patterns. Differentially methylated regions in the promoters of 25 miRNAs overlapped with transposable elements, a finding that may explain the vulnerability of miRNAs to DNA methylation changes during nodule development. Gene expression analysis of a set of promoter-differentially methylated miRNAs pointed to a negative association between DNA methylation and miRNA expression. Gene Ontology and pathways analyses indicate that changes in DNA methylation of miRNA genes are reprogrammed and contribute to nodule development through indirect regulation of genes involved in cellular processes and pathways with well-established roles in nodulation.


2021 ◽  
Author(s):  
Abhinandan Mani Tripathi ◽  
Rajneesh Singh ◽  
Akanksha Singh ◽  
Ashwani Kumar Verma ◽  
Parneeta Mishra ◽  
...  

ABSTRACTSmall RNAs including microRNAs (miRNAs) are short 20-24-nucleotide non-coding RNAs. They are key regulators of gene expression in plants and other organisms. Some small RNAs, mostly 22-nucleotide long trigger biogenesis of secondary small interfering RNAs (siRNAs). Those siRNAs having distinctive phased configuration are known as phased siRNAs (phasiRNAs) and act either in cis or trans enhancing silencing cascade. Here, we report natural variants of MIR158 having deletions or insertions led to negligible or reduced expression of miR158. The deletion/insertion events affected processing of primary transcript of miR158 to precursor and to mature miR158. We show that miR158 targets a pseudo-pentatricopeptide gene and its abolished activity led to 21-nucleotide tertiary phasiRNA generation from its target. The biogenesis of these phasiRNAS is triggered by TAS2 derived two siRNAs. Accordingly, small RNA analyses of these natural variants, mutants and over-expression lines of MIR158 or its target exhibited enhanced or reduced phasiRNA biogenesis. Finally, we functionally validated the highest expressed tertiary phasiRNA that targets NHX2 thereby regulating transpiration and stomatal conductance. Overall, we deciphered a new module of small RNA network, miRNA-TAS-siRNA-pseudogene-tertiary phasiRNA-NHX2, suggesting an additional layer of gene regulation and larger role of pseudogene in plants.


Cells ◽  
2020 ◽  
Vol 9 (10) ◽  
pp. 2327
Author(s):  
Claudia Ghigna ◽  
Maria Paola Paronetto

Alternative splicing generates multiple protein isoforms from one primary transcript and represents one of the major drivers of proteomic diversity in human cells [...]


2020 ◽  
Vol 48 (19) ◽  
pp. 11097-11112
Author(s):  
S Chul Kwon ◽  
Harim Jang ◽  
Siyuan Shen ◽  
S Chan Baek ◽  
Kijun Kim ◽  
...  

Abstract The microprocessor complex cleaves the primary transcript of microRNA (pri-miRNA) to initiate miRNA maturation. Microprocessor is known to consist of RNase III DROSHA and dsRNA-binding DGCR8. Here, we identify Enhancer of Rudimentary Homolog (ERH) as a new component of Microprocessor. Through a crystal structure and biochemical experiments, we reveal that ERH uses its hydrophobic groove to bind to a conserved region in the N-terminus of DGCR8, in a 2:2 stoichiometry. Knock-down of ERH or deletion of the DGCR8 N-terminus results in a reduced processing of suboptimal pri-miRNAs in polycistronic miRNA clusters. ERH increases the processing of suboptimal pri-miR-451 in a manner dependent on its neighboring pri-miR-144. Thus, the ERH dimer may mediate ‘cluster assistance’ in which Microprocessor is loaded onto a poor substrate with help from a high-affinity substrate in the same cluster. Our study reveals a role of ERH in the miRNA biogenesis pathway.


Nature Plants ◽  
2020 ◽  
Vol 6 (10) ◽  
pp. 1262-1274 ◽  
Author(s):  
Ashish Sharma ◽  
Poorwa Kamal Badola ◽  
Chitra Bhatia ◽  
Deepika Sharma ◽  
Prabodh Kumar Trivedi

2020 ◽  
Author(s):  
S. Chul Kwon ◽  
Harim Jang ◽  
Jihye Yang ◽  
Jeesoo Kim ◽  
S. Chan Baek ◽  
...  

ABSTRACTThe Microprocessor complex cleaves the primary transcript of microRNA (pri-miRNA) to initiate miRNA maturation. Microprocessor is known to consist of RNase III DROSHA and dsRNA-binding DGCR8. Here we identify Enhancer of Rudimentary Homolog (ERH) as a new component of the Microprocessor. ERH binds to a conserved region in the N-terminus of DGCR8. Knockdown of ERH or deletion of the DGCR8 N-terminus results in a decrease of processing of primary miRNAs with suboptimal hairpin structures that reside in polycistronic miRNA clusters. ERH increases the processing of suboptimal pri-miR-451 in a manner dependent on its neighboring pri-miR-144. Thus, the ERH dimer may mediate “cluster assistance” in which the Microprocessor is loaded onto a poor substrate with help from a high-affinity substrate in the same cluster. Our study reveals a role of ERH in the miRNA pathway.


2020 ◽  
Vol 66 (4) ◽  
pp. 775-789
Author(s):  
J. Ignacio Moreno ◽  
Ineshia S. Coleman ◽  
Classie L. Johnson ◽  
Dominique S. Green ◽  
Marta A. Piva

2020 ◽  
Vol 36 (9) ◽  
pp. 2926-2928 ◽  
Author(s):  
Warren D Anderson ◽  
Fabiana M Duarte ◽  
Mete Civelek ◽  
Michael J Guertin

Abstract Summary Nascent transcript measurements derived from run-on sequencing experiments are critical for the investigation of transcriptional mechanisms and regulatory networks. However, conventional mRNA gene annotations significantly differ from the boundaries of primary transcripts. New primary transcript annotations are needed to accurately interpret run-on data. We developed the primaryTranscriptAnnotation R package to infer the transcriptional start and termination sites of primary transcripts from genomic run-on data. We then used these inferred coordinates to annotate transcriptional units identified de novo. This package provides the novel utility to integrate data-driven primary transcript annotations with transcriptional unit coordinates identified in an unbiased manner. Highlighting the importance of using accurate primary transcript coordinates, we demonstrate that this new methodology increases the detection of differentially expressed transcripts and provides more accurate quantification of RNA polymerase pause indices. Availability and implementation https://github.com/WarrenDavidAnderson/genomicsRpackage/tree/master/primaryTranscriptAnnotation. Supplementary information Supplementary data are available at Bioinformatics online.


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