RNA-seq comparing the WT mouse hearts versus Dhx36 cKO hearts
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PROVIDER: PRJEB79936 | ENA |
REPOSITORIES: ENA
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Project description:This experiment aimed to investigate the transcriptional role of G4 resolvase Dhx36 in the adult mouse heart. We compared three pools of wild-type (WT) mouse hearts with three pools of Dhx36 conditional knockout (cKO) hearts. In the mutant mice, Dhx36 was conditionally deleted in cardiomyocytes using the Myh6-cre transgenic line. Each of the six pools was created using RNA extracted from 3-5 hearts from mice aged approximately 21 days. The cKO mice developed dilated cardiomyopathy and began experiencing sudden death at 40 days old, with no mutants surviving beyond 5 months.
2024-09-15 | E-MTAB-14440 | biostudies-arrayexpress
Project description:In these experiments, we aimed to investigate the role of cardiomyocyte-specific deletion of the G-quadruplex resolvase Dhx36 in heart development and cardiomyocyte differentiation. To achieve this, we conducted multi-omics analysis using single-nuclei RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) on hearts from postnatal day 7 (PD7) wild-type (WT) and Dhx36 conditional knockout (cKO) mice. Our findings reveal that Dhx36 plays a critical role in the development of the cardiac conduction system (CCS) and in the differentiation of both CCS and working cardiomyocytes
2024-09-15 | E-MTAB-14441 | biostudies-arrayexpress
Project description:In these experiments, we aimed to investigate the role of cardiomyocyte-specific deletion of the G-quadruplex resolvase Dhx36 in heart development and cardiomyocyte differentiation. To achieve this, we conducted multi-omics analysis using single-nuclei RNA sequencing (RNA-seq) and ATAC sequencing (ATAC-seq) on hearts from postnatal day 7 (PD7) wild-type (WT) and Dhx36 conditional knockout (cKO) mice. Our findings reveal that Dhx36 plays a critical role in the development of the cardiac conduction system (CCS) and in the differentiation of both CCS and working cardiomyocytes
2024-09-15 | E-MTAB-14442 | biostudies-arrayexpress
Project description:We generated the cardiac-specific knockout of Trbp (Trbp-cKO) in mice. We profiled the transcriptome in both wild-type and Trbp-cKO hearts, and found numerous genes were deregulated by deletion of Trbp. We also profiled miRNA expression both wild-type and Trbp-cKO hearts, and found expression of a subset of miRNA species was altered in Trbp-cKO hearts. Examine expression of mRNAs and miRNAs in wild-type and Trbp-cKO hearts
2015-04-27 | E-GEOD-67658 | biostudies-arrayexpress
Project description:We generated the cardiac-specific knockout of Trbp (Trbp-cKO) in mice. We profiled the transcriptome in both wild-type and Trbp-cKO hearts, and found numerous genes were deregulated by deletion of Trbp. We also profiled miRNA expression both wild-type and Trbp-cKO hearts, and found expression of a subset of miRNA species was altered in Trbp-cKO hearts.
2015-04-27 | GSE67658 | GEO
Project description:Purpose: Next-generation sequencing (NGS) provides the change of cellular pathways at the transcriptomic level. The overall goal for this research are to compare the transcriptome profiling by NGS in cardiomyocyte-specific FAM210A conditional knockout (cKO) hearts and control (Ctrl) hearts at two different time points and to evaluate the signaling pathways affected by FAM210A deficiency in the heart at the molecular level. Methods: Cardiac mRNA profiles of FAM210A cKO and Ctrl hearts were generated by deep sequencing in triplicate at the late stage (~10 weeks post Fam210a cKO by tamoxifen induction) and in quadruplicates at the early stage (~5 weeks post Fam210a cKO by tamoxifen induction). Results: Using an optimized data analysis workflow from the Genomic Research Center at the University of Rochester, we mapped ~30 millian sequence reads per sample to the mouse genome in the hearts of Ctrl and Fam210a cKO mice at both early and late stages. RNA-seq data comfirmed the knockout of FAM210A in the Fam210a cKO hearts. We identified differentially expressed genes at both early and late stages of FAM210A cKO heart compared with Ctrl hearts (adjust P valuse <0.05). Among upregulated genes, we observed enhanced integrated stress response (ISR) gene signature at both early and late stages in Fam210a cKO hearts compared with Ctrl hearts, including aminoacyl-tRNA synthetases, amino acid synthases, and one-carbon metabolic enzymes. The downregulated genes were not common between the two stages. At the early stage, the top enriched pathways include negative regulation of blood coagulation and wound healing and fatty acid metabolic process. In contrast, at the late stage, the major pathways include sulfide oxidation, glucose import, and mitochondrial ETC complex assembly. Conclusions: Our study provides the first detailed transcriptomic anslysis of cardiomyocyte specific knockout of Fam210a in the heart at two different time-points by NGS. The RNA-seq data reported here provide a framework for comparative investigation of expression profiles in the hearts of FAM210A cKO compared with Ctrl hearts. Based on our analysis, we conclude that ISR is persistently activated in Fam210a cKO hearts, which may be a pro-survival compensatory response caused by the dysfunction of mitochondria in Fam210a cKO hearts. ISR activation can reprogram global cap-dependent translation and cellular metabolism simultaneously.
2023-02-01 | GSE195957 | GEO
Project description:RNA binding proteins can modulate RNA secondary structures, thus participating in post-transcriptional regulation. The DEAH-box helicase 36 (DHX36) has a remarkable ability to bind and unwind RNA G-quadruplex (rG4) and duplex. However, the transcriptome-wide RNA structure dynamic induced by DHX36 and how structure change subsequently influences RNA fate remain poorly understood. Here, we first identify the endogenous binding sites and specificity of DHX36 based on binding profiles. Next, we capture in vivo RNA structuromes to investigate the structure change of DHX36-bound mRNAs following DHX36 knockout. DHX36 induces structure remodeling on not only the localized binding sites but also the other sites across the entire mRNA especially in 3’UTR. DHX36-induced more accessible structures of 3’UTR are revealed to correlate with post-transcriptional mRNA decrease. Furthermore, we demonstrate that DHX36 binding sites are enriched for N6-methyladenosine (m6A) modification and YTHDF1 binding. Finally, we experimentally validate that YTHDF1 binding is repelled to DHX36 loss-induced structure inaccessibility and YTHDF1 loss-induced mRNA stabilization could be a source of DHX36 loss-induced mRNA increase. Altogether, our findings uncover the effect of DHX36 binding on in vivo mRNA structure and propose a plausible mechanism of how RNA secondary structure change involves in post-transcriptional regulation through orchestrating YTHDF1 binding.
2024-10-03 | GSE237159 | GEO
Project description:To identify the YTHDF1 binding changes upon DHX36 loss, we conducted and analyzed YTHDF1 CLIP-seq data in WT and DHX36-KO HEK293T cells.
2024-10-03 | GSE264498 | GEO
Project description:Transcriptional profiling of mouse osteoclasts comparing control osteoclasts from Stat5 flox mice with osteoclasts from Stat5 cKO mice. Two-condition experiment, Stat5 flox cells vs. Stat5 cKO cells
2013-12-09 | E-GEOD-51283 | biostudies-arrayexpress
Project description:RNA binding proteins can modulate RNA secondary structures, thus participating in post-transcriptional regulation. The DEAH-box helicase 36 (DHX36) has a remarkable ability to bind and unwind RNA G-quadruplex (rG4) and duplex. However, the transcriptome-wide RNA structure dynamic induced by DHX36 and how structure change subsequently influences RNA fate remain poorly understood. Here, we first identify the endogenous binding sites and specificity of DHX36 based on binding profiles. Next, we capture in vivo RNA structuromes to investigate the structure change of DHX36-bound mRNAs following DHX36 knockout. DHX36 induces structure remodeling on not only the localized binding sites but also the other sites across the entire mRNA especially in 3’UTR. DHX36-induced more accessible structures of 3’UTR are revealed to correlate with post-transcriptional mRNA decrease. Furthermore, we demonstrate that DHX36 binding sites are enriched for N6-methyladenosine (m6A) modification and YTHDF1 binding. Finally, we experimentally validate that YTHDF1 binding is repelled to DHX36 loss-induced structure inaccessibility and YTHDF1 loss-induced mRNA stabilization could be a source of DHX36 loss-induced mRNA increase. Altogether, our findings uncover the effect of DHX36 binding on in vivo mRNA structure and propose a plausible mechanism of how RNA secondary structure change involves in post-transcriptional regulation through orchestrating YTHDF1 binding.
2024-10-03 | GSE237160 | GEO