Transcription and export complex (THO/TREX) coordinates transcription termination in Arabidopsis
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ABSTRACT:
PROVIDER: PRJNA529202 | ENA |
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| SRR8787250_1.fastq.gz | Fastqsanger.gz | |||
| SRR8787250_2.fastq.gz | Fastqsanger.gz | |||
| SRR8787251.fastq.gz | Fastqsanger.gz | |||
| SRR8787252.fastq.gz | Fastqsanger.gz | |||
| SRR8787253.fastq.gz | Fastqsanger.gz |
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Project description:Transcription termination of mRNAs transcribed from a given locus has a decisive role in regulating the gene function as it determines the coding potential and inclusion of regulatory sequence elements. Failure in appropriate transcription termination leads to read-through transcription, resulting in the synthesis of antisense RNAs which can have profound impact on overall gene expression. However, molecular mechanisms which regulate transcription termination and chimeric RNA formation are poorly understood. We explored the regulatory function of transcription and export complex (THO/TREX) in transcription termination. We show that two members of THO/TREX complex, TREX COMPONENT 1 (TEX1) and HYPER RECOMBINATION1(HPR1) are critical for the correct transcription termination in Arabidopsis. We first demonstrate this by showing defective termination of the bacterial nopaline synthase (NOS) terminator on a transgene in tex1 and hpr1 mutants. Additionally, we show that RNA termination defects in tex1 and hpr1 mutants are widespread at the whole genome levels leading to 3’UTR extensions, truncations and in some cases in the formation of intergenic chimeric transcripts. Chromatin immunoprecipitation coupled with quantitative PCR experiments confirmed the presence of RNA polymerase II beyond the canonical termination sites on genes with defective RNA termination in tex1 and hpr1 mutants. These results demonstrate that THO/TREX complex is a novel regulator of transcription termination in Arabidopsis.
2020-03-24 | GSE128877 | GEO
Project description:THO/TREX is a conserved nuclear complex that functions in mRNP biogenesis at the interface of transcription-RNA export with a key role in preventing transcription-associated genome instability. We used microarrays to analyze the impact of different THO/TREX mutations on gene expression and found that THO-Sub2 deletions have a high functional impact on highly expressed, long and G+C-rich genes regardless of gene function.
2011-06-29 | GSE24802 | GEO
Project description:THO/TREX is a conserved nuclear complex that functions in mRNP biogenesis at the interface of transcription-RNA export with a key role in preventing transcription-associated genome instability. We used microarrays to analyze the impact of different THO/TREX mutations on gene expression and found that THO-Sub2 deletions have a high functional impact on highly expressed, long and G+C-rich genes regardless of gene function. S. cerevisiae strains were grown in YPAD liquid culture, total RNA was isolated and hybridized on Affymetrix microarrays.
2011-06-28 | E-GEOD-24802 | biostudies-arrayexpress
Project description:Transcription termination has important regulatory functions, impacting mRNA stability, localization and translation potential. Failure to appropriately terminate transcription can also lead to read-through transcription and the synthesis of antisense RNAs which can have profound impact on gene expression. The Transcription-Export (THO/TREX) protein complex plays an important role in coupling transcription with splicing and export of mRNA. However, little is known about the role of the THO/TREX complex in the control of transcription termination. In this work, we show that two proteins of the THO/TREX complex, namely TREX COMPONENT 1 (TEX1 or THO3) and HYPER RECOMBINATION1 (HPR1 or THO1) contribute to the correct transcription termination at several loci in Arabidopsis thaliana. We first demonstrate this by showing defective termination in tex1 and hpr1 mutants at the nopaline synthase (NOS) terminator present in a T-DNA inserted between exon 1 and 3 of the PHO1 locus in the pho1-7 mutant. Read-through transcription beyond the NOS terminator and splicing-out of the T-DNA resulted in the generation of a near full-length PHO1 mRNA (minus exon 2) in the tex1 pho1-7 and hpr1 pho1-7 double mutants, with enhanced production of a truncated PHO1 protein that retained phosphate export activity. Consequently, the strong reduction of shoot growth associated with the severe phosphate deficiency of the pho1-7 mutant was alleviated in the tex1 pho1-7 and hpr1 pho1-7 double mutants. Additionally, we show that RNA termination defects in tex1 and hpr1 mutants leads to 3'UTR extensions in several endogenous genes. These results demonstrate that THO/TREX complex contributes to the regulation of transcription termination.
| S-EPMC7179932 | biostudies-literature
Project description:THOC5, a member of the THO complex that is a subcomplex of Transcription/export complex (TREX) 1, is essential for 3´processing of slow kinetics IEGs, and for export of only a subset of genes. Applying nanopore mRNA-sequence technology, we show here that upon depletion of THOC5, 50% of mRNAs showed alteration of 3´end cleavage sites. Moreover, polymerase-II (Pol II)-CHIP-sequencing data reveals that upon depletion of THOC5 Pol II density was increased at gene body and 3´UTR. THOC5 is recruited near to Pol II high density sites except promotor regions, suggesting that THOC5 is involved in transcription elongation. Indeed, 385 THOC5 independent genes in fast Pol II cells became THOC5 dependent in slow Pol II cells. Chromatin associated THOC5 in slow Pol II cells interacts with CDK12, RNA helicases DDX5 and DDX, and THOC6, but not with other members of THO complex. Notably, THOC5 did not form this complex in fast poly II cells. CDK12 was recruited to R-loop (DNA:RNA hybrid) in THOC5/THOC6 dependent manner. Here, THOC6, but not THOC5 directly interacts with R-loop then, recruited DDX5 resolves R-loop and then CDK12 enhances further transcription elongation. These data show for the first time the novel function of THOC5/THOC6 complex during transcription elongation.
2022-12-31 | GSE166115 | GEO
Project description:N6-methyladenosine (m6A) is the most abundant internal modification of eukaryotic mRNA. This modification has previously been shown to alter the export kinetics for mRNAs though the molecular details surrounding this phenomenon remain poorly understood. Here we show that the m6A complex (WTAP, KIAA1429, METTL3/14) drives recruitment of the TREX mRNA export complex onto m6A modified mRNAs and this process is essential for the efficient export of certain mRNAs. Depletion of the core m6A complex leads to loss of TREX from mRNAs which undergo the m6A modification. We show that TREX stimulates recruitment of the m6A reader protein YTHDC1 to the mRNP and the m6A complex influences the interaction of TREX with YTHDC1. We suggest that m6A acts as a surrogate for other TREX recruitment mechanisms such as splicing and 5’ capping, in long internal and final exons which may otherwise be devoid of this essential complex for mRNA export.
2018-10-03 | GSE111878 | GEO
Project description:THOC6 is the genetic basis of autosomal recessive THOC6 Intellectual Disability Syndrome (TIDS). THOC6 is critical for mammalian Transcription Export complex (TREX) tetramer formation, which is composed of four six-subunit THO monomers. The TREX tetramer facilitates mammalian RNA processing, in addition to the nuclear mRNA export functions of the TREX dimer conserved through yeast. Human and mouse TIDS model systems revealed novel THOC6-dependent, species-specific TREX tetramer functions. Germline biallelic Thoc6 loss-of-function (LOF) variants result in mouse embryonic lethality. Biallelic THOC6 LOF variants do not alter the expression of TREX dimer component proteins in human cells, but reduced binding affinity to ALYREF implicates impaired TREX tetramer formation. Defects in RNA nuclear export functions were not detected in biallelic THOC6 LOF human neural cells. Instead, mis-splicing was detected in human and mouse neural tissue, revealing novel THOC6-mediated TREX coordination of mRNA processing. We demonstrate that THOC6 is required for regulation of key signaling pathways in human corticogenesis that dictate the transition from proliferative to neurogenic divisions, developmental biology implicated in TIDS neuropathology.
2023-10-17 | GSE245121 | GEO
Project description:The conserved THO/TREX complex is critical for pre-mRNA processing and mRNA nuclear export. In Metazoa, TREX is loaded on nascent RNA transcribed by RNA polymerase II in a splicing-dependent fashion; however, how TREX functions is poorly understood. Here we show that Thoc5 and other TREX components are essential for the biogenesis of piRNA, a distinct class of small non-coding RNAs that control expression of transposable elements (TE) in the Drosophila germline. Mutations in TREX lead to defects in piRNA biogenesis resulting in derepression of multiple TE families, gametogenesis defects, and sterility. TREX components are enriched on piRNA precursors transcribed from dual-strand piRNA clusters and co-localize in distinct nuclear foci that overlap with sites of piRNA transcription. The localization of TREX in nuclear foci and its loading on piRNA precursor transcripts depends on Cutoff, a protein associated with chromatin of piRNA clusters. Finally, we show that TREX is required for accumulation of nascent piRNA precursors. Our study reveals a novel splicing-independent mechanism for TREX loading on nascent RNA and its importance in piRNA biogenesis.
2016-03-18 | GSE79325 | GEO
Project description:THO/TREX is a conserved nuclear complex that functions in mRNP biogenesis and prevents transcription-associated recombination. Whether or not it has a ubiquitous role in the genome is an open question. ChIP-chip studies reveal that the Hpr1 component of THO and the Sub2 RNA-dependent ATPase have genome wide-distributions at active ORFs in yeast. In contrast to RNAPII, evenly distributed from promoter to termination regions, THO and Sub2 are absent at promoters and distributed in a sharp 5M-bM-^@M-^YM-bM-^FM-^R3M-bM-^@M-^Y gradient. Importantly, ChIP-chips reveal an over-recruitment of Rrm3 in active genes in THO mutants that is reduced by overexpression of RNase H1. Our work establishes a genome-wide function for THO-Sub2 in transcription elongation and mRNP biogenesis that function to prevent the accumulation of transcription-mediated replication obstacles, including R-loops. ChIP-chip studies were perfomed with tagged forms of the Hpr1 component of THO (Hpr1-FLAG), the Sub2 RNA-dependent ATPase of TREX (Sub2-FLAG), the Rpb3 subunit of RNA polymerase II (Rpb3-PK) and the Rrm3 protein (Rrm3-FLAG) in the yeast S. cerevisiae.
2011-06-28 | E-GEOD-24960 | biostudies-arrayexpress
Project description:TREX (Transcription-Export) is a highly conserved multi-subunit protein complex that, besides its established role in mRNA export from nucleus to cytoplasm, is involved in transcriptional regulation, stem cell maintenance, 3’ mRNA processing, mitotic progression, and genome stability in eukaryotic cells. TREX is composed of a six subunit THO core complex (THOC1, THOC2, THOC3, THOC5, THOC6 and THOC7) and eight accessory proteins. We have implicated the X-chromosome THOC2 gene, which encodes the scaffold protein of the THO complex, in a clinically variable neurodevelopmental disorder (NDD) with intellectual disability (ID) as the core phenotype. To study the function of this essential eukaryotic gene and the mechanisms underlying its NDD outcomes, we generated a clinically-relevant mouse model based on a hypomorphic Thoc2 exon37-38 deletion variant of a patient with ID, speech delay, hypotonia, and microcephaly. The Thoc2 exon37-38 deletion male (Thoc2Δ/Y) mice recapitulate the core phenotypes of THOC2 syndrome including smaller size and weight, and significant deficits in spatial learning, working memory and sensorimotor functions. The Thoc2Δ/Y mice brain development is significantly impacted by compromised THOC2/TREX function resulting in R-loop accumulation, DNA damage and consequent cell death. Differentiated cortical neurons of Thoc2Δ/Y mice show perturbed synaptic and electrophysiological properties underlined by increased DNA damage comparable to the primary cells of patients with THOC2 pathogenic variants. Altogether, our data suggest that perturbed R-loop homeostasis, in stem cells and/or differentiated cells in mice and men, and DNA damage-associated functional alterations are at the root of THOC2 syndrome. Overall, we suggest that THOC2 is a major, conserved player in the efficient resolution of R-loops, a process essential for normal brain development and function.
2023-12-15 | GSE245539 | GEO