Ectopic histone modification in extra-embryonic tissues influence implantation and placenta development of IVF embryos [RNA-Seq 3]
Ontology highlight
ABSTRACT:
ORGANISM(S): Mus musculus
PROVIDER: GSE197914 | GEO | 2022/05/26
REPOSITORIES: GEO
Similar Datasets
Project description:To further investigate the relationship between abnormal accumulation of H3K4me3 modification and abnormal embryo development. We injected Kdm5b siRNA, which is an H3K4me3 eraser, at the zygote (PN3-PN4) stage of NM embryos and then examined the H3K4me3 modification of extraembryonic ectoderm at E7.5.
2022-05-26 | GSE197920 | GEO
Project description:Assisted reproductive technology (ART), especially in vitro fertilization (IVF) and embryo transfer have been widely applied in the treatment of human infertility. However, the accumulating evidences indicate that IVF is associated with low pregnancy rate, placental defect and the metabolic diseases in offspring. Here, we identify ectopic histone H3K4me3 in extraembryonic ectoderm (ExE) as an important reason for embryo implantation failure and extra-embryonic development abnormalities of IVF embryos. IVF manipulation notably disrupt extra-embryonic tissue-specific gene expression, 334 epiblast (Epi)-specific genes and 24 Epi-specific transcription factors were abnormally expressed in ExE of IVF embryos at embryonic day 7.5 (E7.5). Combined histone modification analysis reveal that ectopic H3K4me3 modification at the Epi-active promoter resulted in increased expression of these genes in ExE of IVF embryos at E7.5. By konckdown the expression of H3K4me3 recruited regulator Kmt2e, which highly expressed in IVF embryos, can improve the development of IVF embryo and reduce the abnormal gene expression in ExE. Therefore, our research identifies the abnormal H3K4me3 modification occupied in extra-embryonic tissue may be an important reason for implantation failure and abnormal placental development of IVF embryo.
2022-05-26 | GSE168269 | GEO
Project description:Assisted reproductive technology (ART), especially in vitro fertilization (IVF) and embryo transfer have been widely applied in the treatment of human infertility. However, the accumulating evidences indicate that IVF is associated with low pregnancy rate, placental defect and the metabolic diseases in offspring. Here, we identify ectopic histone H3K4me3 in extraembryonic ectoderm (ExE) as an important reason for embryo implantation failure and extra-embryonic development abnormalities of IVF embryos. IVF manipulation notably disrupt extra-embryonic tissue-specific gene expression, 334 epiblast (Epi)-specific genes and 24 Epi-specific transcription factors were abnormally expressed in ExE of IVF embryos at embryonic day 7.5 (E7.5). Combined histone modification analysis reveal that ectopic H3K4me3 modification at the Epi-active promoter resulted in increased expression of these genes in ExE of IVF embryos at E7.5. By konckdown the expression of H3K4me3 recruited regulator Kmt2e, which highly expressed in IVF embryos, can improve the development of IVF embryo and reduce the abnormal gene expression in ExE. Therefore, our research identifies the abnormal H3K4me3 modification occupied in extra-embryonic tissue may be an important reason for implantation failure and abnormal placental development of IVF embryo.
2022-05-26 | GSE168272 | GEO
Project description:Assisted reproductive technology (ART), especially in vitro fertilization (IVF) and embryo transfer have been widely applied in the treatment of human infertility. However, the accumulating evidences indicate that IVF is associated with low pregnancy rate, placental defect and the metabolic diseases in offspring. Here, we identify ectopic histone H3K4me3 in extraembryonic ectoderm (ExE) as an important reason for embryo implantation failure and extra-embryonic development abnormalities of IVF embryos. IVF manipulation notably disrupt extra-embryonic tissue-specific gene expression, 334 epiblast (Epi)-specific genes and 24 Epi-specific transcription factors were abnormally expressed in ExE of IVF embryos at embryonic day 7.5 (E7.5). Combined histone modification analysis reveal that ectopic H3K4me3 modification at the Epi-active promoter resulted in increased expression of these genes in ExE of IVF embryos at E7.5. By konckdown the expression of H3K4me3 recruited regulator Kmt2e, which highly expressed in IVF embryos, can improve the development of IVF embryo and reduce the abnormal gene expression in ExE. Therefore, our research identifies the abnormal H3K4me3 modification occupied in extra-embryonic tissue may be an important reason for implantation failure and abnormal placental development of IVF embryo.
2022-05-26 | GSE168273 | GEO
Project description:This SuperSeries is composed of the SubSeries listed below.
2022-05-25 | GSE168274 | GEO
Project description:ES cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in iPS cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation, and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency-genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process. ChIP-Seq for H3K4me3 and H3K4me2 in murine shLuc and shKdm5b 4TF-MEFs (tetO-Pou5f1,-Sox2,-Klf4,-c-Myc) at 48h.
2013-10-14 | E-GEOD-47123 | biostudies-arrayexpress
Project description:Ectopic histone modification in extra-embryonic tissues influence implantation and placenta development of IVF embryos
| PRJNA706709 | ENA
Project description:ES cell pluripotency is thought to be regulated in part by H3K4 methylation. However, it is unclear how H3K4 demethylation contributes to ES cell function and participates in iPS cell reprogramming. Here, we show that KDM5B, which demethylates H3K4, is important for ES cell differentiation, and presents a barrier to the reprogramming process. Depletion of Kdm5b leads to an extension in the self-renewal of ES cells in the absence of LIF. Transcriptome analysis revealed the persistent expression of pluripotency-genes and underexpression of developmental genes during differentiation in the absence of Kdm5b, suggesting that KDM5B plays a key role in cellular fate changes. We also observed accelerated reprogramming of differentiated cells in the absence of Kdm5b, demonstrating that KDM5B is a barrier to the reprogramming process. Expression analysis revealed that mesenchymal master regulators associated with epithelial-to-mesenchymal transition (EMT) are downregulated during reprogramming in the absence of Kdm5b. Moreover, global analysis of H3K4me3/2 revealed that enhancers of fibroblast genes are rapidly deactivated in the absence of Kdm5b, and genes associated with EMT lose H3K4me3/2 during the early reprogramming process. These findings provide functional insight into the role for KDM5B in regulating ES cell differentiation and as a barrier to the reprogramming process. RNA-Seq of undifferentiated and embryoid body (EB) differentiated murine shLuc and shKdm5b ES cells
2013-10-14 | E-GEOD-47124 | biostudies-arrayexpress
Project description:The H3K4 demethylase KDM5B is overexpressed in multiple cancer types, but the underlying mechanistic contribution of dysregulated H3K4 demethylation in cancer is poorly understood. Here, we show that depletion of KDM5B in multiple types of cancer cells leads to increased proliferation, decreased heterogeneity, and phenotype changes consistent with a de-differentiated or stem cell-like phenotype. Our results also support a role for KDM5B in regulating epigenetic plasticity, where loss of KDM5B in cancer cell lines with elevated KDM5B expression leads to permissive or repressive chromatin states, which facilitate activation or repression of alternative transcriptional programs. KDM5B depleted cancer cells exhibited altered epigenetic and transcriptional profiles resembling a more primitive cellular state. Genome-wide maps of H3K4me3 across a compendium of KDM5B-depleted cancer cell lines revealed altered distributions of canonical and broad H3K4me3 domains at promoters of tumor suppressors. Genes with altered H3K4me3 in KDM5B-depleted cancer cells were enriched with tumor suppressors and housekeeping genes. While high expression of KDM5B is associated with poor clinical outcomes, findings from this study suggest that targeted inhibition of KDM5B as a therapeutic strategy may not be sufficient to inhibit growth of cancer cells as KDM5B regulates H3K4 methylation at a wide range of genes, but does so in a context-dependent manner. This study also provides a resource for evaluating associations between alterations in epigenetic patterning of H3K4 methylation and transcriptome profiles in a diverse set of cancer cells.
2022-05-19 | GSE165958 | GEO
Project description:The H3K4 demethylase KDM5B is overexpressed in multiple cancer types, but the underlying mechanistic contribution of dysregulated H3K4 demethylation in cancer is poorly understood. Here, we show that depletion of KDM5B in multiple types of cancer cells leads to increased proliferation, decreased heterogeneity, and phenotype changes consistent with a de-differentiated or stem cell-like phenotype. Our results also support a role for KDM5B in regulating epigenetic plasticity, where loss of KDM5B in cancer cell lines with elevated KDM5B expression leads to permissive or repressive chromatin states, which facilitate activation or repression of alternative transcriptional programs. KDM5B depleted cancer cells exhibited altered epigenetic and transcriptional profiles resembling a more primitive cellular state. Genome-wide maps of H3K4me3 across a compendium of KDM5B-depleted cancer cell lines revealed altered distributions of canonical and broad H3K4me3 domains at promoters of tumor suppressors. Genes with altered H3K4me3 in KDM5B-depleted cancer cells were enriched with tumor suppressors and housekeeping genes. While high expression of KDM5B is associated with poor clinical outcomes, findings from this study suggest that targeted inhibition of KDM5B as a therapeutic strategy may not be sufficient to inhibit growth of cancer cells as KDM5B regulates H3K4 methylation at a wide range of genes, but does so in a context-dependent manner. This study also provides a resource for evaluating associations between alterations in epigenetic patterning of H3K4 methylation and transcriptome profiles in a diverse set of cancer cells.
2022-05-19 | GSE165957 | GEO