Next Generation Sequencing Facilitates Quantitative Analysis of PHB-knockdown and PHB-knockout Spermatocytes Transcriptomes
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE140346 | GEO | 2020/04/02
REPOSITORIES: GEO
Similar Datasets
Project description:Next Generation Sequencing Facilitates Quantitative Analysis of PHB-knockdown and PHB-knockout Spermatocytes Transcriptomes
| PRJNA589316 | ENA
Project description:Prohibitin (PHB) plays a significant role in cancer processes whereas its mechanism in bladder cancer (BC) aggressiveness is not fully understood. This study aimed to investigate the role of PHB in BC aggressiveness. The study employed a range of in vivo and in vitro assays to elucidate the interaction between PHB-NADSYN1 and its underlying function in BC progression. We found that PHB was upregulated in muscle-invasive bladder cancer tissues, and bound to NADSYN1 mRNA in BC tissues more than in adjacent normal tissues. NADSYN1 and PHB were upregulated and positively correlated both in BC tissues and cell lines. We further revealed that deleting NADSYN1 prevented PHB-mediated cell invasiveness of BC in vivo and in vitro. PHB could directly bind to NADSYN1 mRNA, and it was found that the PHB domain was responsible for the PHB-NADSYN1 interaction. Depletion of NADSYN1 expression significantly decreased the protein level of PHB. In addition, Snai2 positively correlated with NADSYN1 and depletion or mutation of Snai2 binding sites inhibited NADSYN1-PHB-mediated BC progression. The study highlights a novel Snai2-NADSYN1-PHB mechanism in BC progression and indicates that PHB and NADSYN1 could serve as a therapeutic target for BC
2024-01-24 | GSE243441 | GEO
Project description:Embryonic stem cells (ESCs) are useful resources for clinical cell therapy as its unlimited self- renewal and pluripotecy properties, so it is critical to understand how ESCs maintain its identity. We reported a gene named PHB is essential for hESC self- renewal. We used microarrays to find out the potential mechanisms regulated by PHB in maintaining hESC identity.
2016-11-30 | GSE71765 | GEO
Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of α-ketoglutarate (α-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for α-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination. Examination of H3.3 deposition in NT, PHB, and HIRA siRNA treated hESCs respectively.
2016-08-11 | E-GEOD-72143 | biostudies-arrayexpress
Project description:Transcriptional profiling of Haloarcula hispanica comparing PHB with 960. PHB represents the PHA synthase genes mutant (i.e., M-NM-^TphaEC) which is deficient in PHBV accumulation when grown in MG medium. 960 represents the wild-type strain which can produce PHBV when grown in MG medium. Goal was to explore the PHBV biosynthesis and its impact on central metabolism in H. hispanica. Total RNA from PHB and 960 were used to generate target cDNA, and then hybridized to 8*15K Haloarcula hispanica genome array genechips, representing about 3800 genes.
2013-01-22 | E-GEOD-42799 | biostudies-arrayexpress
Project description:Transcriptional profiling of Haloarcula hispanica comparing PHB with 960. PHB represents the PHA synthase genes mutant (i.e., ΔphaEC) which is deficient in PHBV accumulation when grown in MG medium. 960 represents the wild-type strain which can produce PHBV when grown in MG medium. Goal was to explore the PHBV biosynthesis and its impact on central metabolism in H. hispanica.
2013-01-22 | GSE42799 | GEO
Project description:Cellular metabolism and chromatin landscape both contribute to cell fate determination. However, their interplay remains poorly understood. Here we show that Prohibitin (PHB), an evolutionarily conserved protein, involves in a histone variant H3.3 chaperon HIRA complex-dependent epigenetic and metabolic circuitry to maintain the identity of human embryonic stem cells (hESCs). We found that silencing of PHB triggers hESC differentiation with concomitant enhancements of histone 3 (H3) lysine (K) methyl modifications as a result of the reduced production of α-ketoglutarate (α-KG), a metabolite required for activities of many dioxygenase and in turn chromatin structure1,2. Mechanistically, PHB acts as a functional member of the HIRA complex3,4. Resembling PHB deficiency, loss of HIRA in hESCs leads to massive differentiation and aberrant histone modifications, although it was previously found not to disrupt the self-renewal in mouse ESCs (mESCs)5. Genome-wide H3.3 ChIP- sequence analyses indicate that reduction of H3.3 deposition caused by PHB knock down is extremely similar to that induced by HIRA knock down. Specifically, silencing either HIRA or PHB leads to repressive chromatin characters at promoters of pluripotency genes and isocitrate dehydrogenases (IDHs), the enzyme responsible for α-KG production, but active chromatin features at promoters of developmental genes, paralleling to transcript levels of these genes. Our results identify PHB as an essential factor not only for hESC self-renewal but also for the proper function of the HIRA complex, linking the HIRA complex-dependent H3.3 deposition to the production of a critical metabolite required for shaping chromatin structure, and demonstrating the importance of the interplay between epigenetic state and metabolic regulation in cell fate determination.
2016-08-11 | GSE72143 | GEO
Project description:Peribacillus butanolivorans strain:PHB-7a Genome sequencing
| PRJNA480542 | ENA
Project description:Expression profiling of isolated populations of prepachytene spermatocytes (LP), pachytene spermatocytes (RP) and spermatids (ST) from PWD and B6 was performed to study the genome wide variation in gene expression between two mouse subspecies. To evaluate the transcriptional difference between B6 and PWD in during meiosis, we compared their transcriptomes in sorted populations of pre-pachytene primary spermatocytes (Leptonema, Zygotene and Pachytene), pachytene spermatocytes (Mid-late pachytene and diplotene) and spermatids. Populations of pre-pachytene spermatocytes, pachytene spermatocytes and spermatids were isolated from PWD and B6 mice. All populations were isolated in duplicates from two animals. Hence, RNA was prepared from 12 samples (= 2 strains x 3 tissues x 2 replicas) and was then subject to labeling and hybridization on microarray chips.
2014-06-01 | E-GEOD-49444 | biostudies-arrayexpress
Project description:Gas fermentation is emerging as an economically attractive option for the sustainable production of fuels and chemicals from gaseous waste feedstocks. Clostridium autoethanogenum can use CO and/or CO2 + H2 as its sole carbon and energy sources. Fermentation of C. autoethanogenum is currently being deployed on a commercial scale for ethanol production. Expanding the product spectrum of acetogens will enhance the economics of gas fermentation. To achieve efficient heterologous product synthesis, limitations in redox and energy metabolism must be overcome. Here, we engineered and characterised at a systems-level, a recombinant poly-3-hydroxybutyrate (PHB)-producing strain of C. autoethanogenum. Cells were grown in CO-limited steady-state chemostats on two gas mixtures, one resembling syngas (20% H2) and the other steel mill off-gas (2% H2). Results were characterised using metabolomics and transcriptomics, and then integrated using a genome-scale metabolic model reconstruction. PHB-producing cells had an increased expression of the Rnf complex, suggesting energy limitations for heterologous production. Subsequent optimisation of the bioprocess led to a 12-fold increase in the cellular PHB content. The data suggest that the cellular redox state, rather than the acetyl-CoA pool, was limiting PHB production. Integration of the data into the genome-scale metabolic model showed that ATP availability limits PHB production. Altogether, the data presented here advances the fundamental understanding of heterologous product synthesis in gas-fermenting acetogens.
2019-02-03 | GSE115837 | GEO