| 2004 |
Drosophila THO complex is composed of THO2, HPR1, THOC5, THOC6, and THOC7 (the latter three having no orthologs in budding yeast). Depletion of THO components showed that export of heat-shock mRNAs under heat stress is strictly dependent on THO function, while <20% of the transcriptome is regulated by THO under normal conditions. |
Gene expression profiling (microarray) in Drosophila cells depleted of THO components; RNAi knockdown |
Nature structural & molecular biology |
Medium |
15133499
|
| 2008 |
THOC7 does not contain a nuclear localization signal and resides mainly in the cytoplasm in the absence of FMIP (THOC5). THOC7 (amino acids 50–137) directly binds the N-terminal portion (aa 1–199) of FMIP, and this interaction is required for THOC7 nuclear localization; a THOC7 mutant lacking the FMIP-binding site fails to co-localize with FMIP in the nucleus. |
Co-immunoprecipitation, deletion mapping, fluorescence microscopy (co-localization), direct binding assay |
FEBS letters |
Medium |
19059247
|
| 2011 |
THOC7 is a component of the mammalian THO subcomplex (together with THOC1, THOC2, THOC5, THOC6), which is part of the TREX complex required for nuclear export of specific mRNAs. In THOC5-knockout mouse embryo fibroblasts, 10 genes were identified that were spliced but not exported to the cytoplasm; these mRNAs co-purified with THOC5, placing THO at the mRNA export step. Hsp70 mRNA export required THOC5 under heat shock (42°C) but not under normal conditions (37°C). |
Conditional knockout (Cre/lox), transcriptome analysis of cytoplasmic RNA, RNA co-immunoprecipitation with THOC5 |
RNA (New York, N.Y.) |
Medium |
21525145
|
| 2018 |
In Drosophila, mutations in thoc7 (and thoc5) disrupt interactions among the remaining THO subunits and reduce UAP56 binding to the core THO subunit Hpr1, thereby disrupting piRNA precursor complex assembly. THOC7 mutations are viable but cause sterility and impair piRNA biogenesis. Furthermore, thoc7 mutations reduce Rhino (HP1 homolog) binding to piRNA clusters and trigger ectopic Rhino binding across the genome, demonstrating that THO complexes restrict Rhino localization to cluster heterochromatin. |
Genetic epistasis (viable thoc7 mutations), co-immunoprecipitation (subunit interaction mapping), germline sterility assay, ChIP for Rhino |
Cell reports |
High |
30257203
|
| 2019 |
THOC7 negatively regulates the cellular antiviral innate immune response by promoting K48-linked polyubiquitination and proteasomal degradation of TBK1. THOC7 overexpression inhibited Sendai virus- or polyI:C-induced IRF3 dimerization/phosphorylation and IFN-β production, while THOC7 knockdown had opposite effects. THOC7 was found to associate with the MAVS signalosome and acts at the TBK1 level of the RLR/MAVS signaling cascade. |
Overexpression and knockdown (siRNA), co-immunoprecipitation (MAVS signalosome), ubiquitination assay (K48 polyubiquitination), IRF3 dimerization/phosphorylation assay, IFN-β reporter assay |
Viruses |
Medium |
30769920
|
| 2020 |
Human THOC7 occupies repetitive genomic sequences (microsatellite repeats in genic/intergenic regions and telomeric repeats) as determined by ChIP-seq; THOC7 ChIP peaks overlap with those of elongating RNA Pol II and R-loops, indicating accumulation at transcriptionally active repeat regions. Knockdown of THOC5 (an RNA-binding THO subunit) induces γH2AX accumulation at repeat regions and telomere aberrations, linking the THO complex to maintenance of genome stability at repetitive sequences. |
Chromatin immunoprecipitation sequencing (ChIP-seq) of THOC7, siRNA knockdown of THOC5, γH2AX immunofluorescence, R-loop co-localization |
Genes to cells : devoted to molecular & cellular mechanisms |
Medium |
32065701
|
| 2014 |
Depletion of THOC7 (along with THOC5) selectively reduced the level of unspliced (but not spliced) murine leukemia virus (MLV) transcripts in the cytoplasm, and THOC5 RNA immunoprecipitation showed association specifically with the unspliced viral transcript, placing THOC7/THOC5 in the nuclear export pathway for unspliced viral RNAs via the NXF1 pathway. |
siRNA knockdown of THOC7/THOC5, cytoplasmic RNA quantification, RNA immunoprecipitation (THOC5) |
Viruses |
Medium |
24618812
|
| 2021 |
In Drosophila, null thoc7 mutations displace Thoc5 and Thoc6 from a Tho2-Hpr1 subcomplex. Despite reducing expression of a subset of germline piRNAs and increasing transposon transcription, thoc7-null mutations do not reduce anti-sense piRNAs targeting half of the activated transposon families, do not reduce piRNA-guided H3K9me3, and do not block Panoramix-dependent silencing of a reporter. Unspliced transposon transcripts co-precipitate with THO through a Piwi- and Panoramix-independent mechanism. Piwi mutations dominantly enhance germline defects in thoc7-null alleles, establishing that THO acts in a piRNA-independent transposon-silencing pathway cooperatively with Piwi. |
Genetic epistasis (null thoc7 alleles, piwi mutations, double mutants), RNA co-immunoprecipitation (transposon transcript-THO), H3K9me3 ChIP, piRNA sequencing, reporter transgene assay |
Developmental cell |
High |
34547226
|
| 2022 |
THOC7 directly binds lncRNA Pnky as confirmed by colocalization and RNA immunoprecipitation (RIP) assays, and this interaction is proposed to couple mRNA splicing and nuclear export of NSC migration-related mRNAs. |
RNA immunoprecipitation (RIP), colocalization assay |
Cellular and molecular neurobiology |
Low |
35748966
|
| 2026 |
In Drosophila, thoc7 mutations (which disrupt piRNA precursor binding to the THO complex) delay RDC (Rhino-Deadlock-Cuff) relocalization to piRNA clusters after acute heat shock, while piwi mutations accelerate it. This places THOC7-dependent THO complex assembly upstream of RDC cluster reassembly after stress, and demonstrates that maternally deposited piRNAs are dispensable for RDC localization to the major 42AB cluster. |
Genetic epistasis (thoc7 mutants, piwi mutants), live imaging of RDC localization, fluorescence microscopy after heat shock recovery |
RNA (New York, N.Y.) |
Medium |
41397876
|