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THAP1 is a master regulator of zinc finger transcription factors guiding gastrulation of murine embryos [scRNA-seq_rat]

ABSTRACT: Gastrulation and early organogenesis are remarkable processes of early embryonic development. Our previous study showed that deletion of DYT6 gene product THAP1 leads to embryonic lethality at the stage of gastrulation and early organogenesis. However, the function of THAP1 in regulating gene expression, as well as its role in regulating embryo gastrulation and early organogenesis are not well characterized. In this study, we used different in vitro and in vivo models to characterize the function of THAP1 in regulating gene expression and in controlling embryonic development, which could help us to understand pathogenesis of THAP1-associated disorders and provide data to characterize the transcription regulation of gastrulation of murine embryo.

ORGANISM(S): Rattus norvegicus

PROVIDER: GSE234678 | GEO | 2024/08/01

REPOSITORIES: GEO

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THAP1 is a master regulator of zinc finger transcription factors guiding gastrulation of murine embryos [ChIP-seq_SH]

Project description:Gastrulation and early organogenesis are remarkable processes of early embryonic development. Our previous study showed that deletion of DYT6 gene product THAP1 leads to embryonic lethality at the stage of gastrulation and early organogenesis. However, the function of THAP1 in regulating gene expression, as well as its role in regulating embryo gastrulation and early organogenesis are not well characterized. In this study, we used different in vitro and in vivo models to characterize the function of THAP1 in regulating gene expression and in controlling embryonic development, which could help us to understand pathogenesis of THAP1-associated disorders and provide data to characterize the transcription regulation of gastrulation of murine embryo.

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THAP1 is a master regulator of zinc finger transcription factors guiding gastrulation of murine embryos [RNA-seq_mESC]

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THAP1 is a master regulator of zinc finger transcription factors guiding gastrulation of murine embryos [RNA-seq_SH]

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THAP1 is a master regulator of zinc finger transcription factors guiding gastrulation of murine embryos [ChIP-seq(mESC)]

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Transcriptomic analysis of conditional THAP1 knockout mice brains using microarray

Project description:Loss of function mutations in the transcription factor THAP1 cause DYT6 dystonia, a childhood-onset motor disorder. DYT6 subjects display abnormalities in the white matter regions of the brain. Here, we generated conditional THAP1 knockout mice and analyzed the gene expression profiles from motor regions of mice brains to identify a role for THAP1 in the control of myelination

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THAP1 is cell type dependent regulator of SP1 family crucial for dystonic syndromes in human and rat [SHSY5Y_ChIP-seq]

Project description:THAP1 is a transcription factor and its mutations are responsible for DYT6 dystonia. However, how THAP1 mutations lead to these gene expression alterations and whether the gene expression changes are also reflected in the brain of THAP1 patients are still unclear. In this study we used epigenetic and transcriptomic approaches combined with multiple model systems to uncover the function of THAP1 and the potential pathogenesis of DYT6 dystonia. THAP1 mutations lead to dysregulation of genes mainly through regulation of SP1 family members, SP1 and SP4, in a cell type dependent manner.

2022-09-28 | GSE184957 | GEO

THAP1 is cell type dependent regulator of SP1 family crucial for dystonic syndromes in human and rat [Striatum_RNA-seq]

2022-09-28 | GSE184959 | GEO

THAP1 is cell type dependent regulator of SP1 family crucial for dystonic syndromes in human and rat [SHSY5Y_RNA-seq]

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Transcriptomic analysis of THAP1 mediated oligodendrocyte development

Project description:We demonstrated previously that THAP1 plays a cell-autonomous role in regulating myelination during early postnatal CNS development (Yellajoshyula et al., Dev Cell, 42, 52-67, 2017). To begin to examine the mechanisms responsible for this role, we performed RNAseq at multiple time points on cultured control (Thap1+/+) and Thap1 null (derived from Thap1flx/-; Olig2-Cre+) OPC under differentiating conditions.

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The Dystonia Gene THAP1 Controls DNA Double Strand Break Repair Choice [ChIP-Seq]

Project description:The Shieldin complex, consisting of SHLD1, SHLD2, SHLD3 and REV7, shields double strand DNA breaks (DSBs) from nucleolytic resection. The end-protecting activity of Shieldin promotes productive non-homologous end joining (NHEJ) in G1 but can threaten genome integrity during S-phase by blocking homologous recombination (HR). Curiously, the penultimate Shieldin component, SHLD1 is one of the least abundant mammalian proteins. Here, we report that the transcription factors THAP1, YY1 and HCF1 bind directly to the SHLD1 promoter, where they cooperatively maintain the low basal expression of SHLD1. Functionally, this transcriptional network ensures that SHLD1 protein levels are kept in check to enable a proper balance between end protection and end resection during physiological DSB repair. In the context of BRCA1 deficiency, loss of THAP1 dependent SHLD1 expression confers cross resistance to PARP inhibitor and cisplatin, and shorter progression free survival in ovarian cancer patients. In contrast, loss of THAP1 in BRCA2 deficient cells increases genome instability and correlates with improved responses to chemotherapy. Pathogenic THAP1 mutations are causatively linked to adult-onset torsion dystonia type 6 (DYT6) movement disorder, but the critical disease targets are unknown. We further demonstrate that murine models of Thap1-associated dystonia show reduced Shld1 expression concomitant with elevated levels of unresolved DNA damage in the brain. In summary, our study provides the first example of a transcriptional network that directly controls DSB repair choice and reveals a previously unsuspected link between DNA damage and dystonia.

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