Xenopus laevis
Ontology highlight
ABSTRACT:
PROVIDER: PRJNA176360 | ENA |
REPOSITORIES: ENA
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Project description:Post-translational modifications (PTMs) of histones exert fundamental roles in regulating gene expression. During development, groups of PTMs are constrained by unknown mechanisms into combinatorial patterns, which facilitate transitions from uncommitted embryonic cells into differentiated somatic cell lineages. Repressive histone modifications such as H3K9me3 or H3K27me3 have been investigated in detail, but the role of H4K20me3 in development is currently unknown. Here we show that Xenopus laevis Suv4-20h1 and h2 histone methyltransferases (HMTases) are essential for induction and differentiation of the neuroectoderm. Morpholino-mediated knockdown of the two HMTases leads to a selective and specific downregulation of genes controlling neural induction, thereby effectively blocking differentiation of the neuroectoderm. Global transcriptome analysis supports the notion that these effects arise from the transcriptional deregulation of specific genes rather than widespread, pleiotropic effects. Interestingly, morphant embryos fail to repress the Oct4-related Xenopus gene Oct-25. We validate Oct-25 as direct target of xSu4-20h enzyme-mediated gene repression, showing by chromatin immunoprecipitaton that it is decorated with the H4K20me3 mark downstream of the promoter in normal, but not in double-morphant, embryos. Since knockdown of Oct-25 protein significantly rescues the neural differentiation defect in xSuv4-20h double-morphant embryos, we conclude that the epistatic relationship between Suv4- 20h enzymes and Oct-25 controls the transit from pluripotent to differentiation-competent neural cells. Consistent with these results in Xenopus, murine Suv4-20h1/h2 double-knockout embryonic stem (DKO ES) cells exhibit increased Oct4 protein levels before and during EB formation, and reveal a compromised and biased capacity for in vitro differentiation, when compared to normal ES cells. Together, these results suggest a regulatory mechanism, conserved between amphibian and mammals, in which H4K20me3-dependent restriction of specific POU-V genes directs cell fate decisions, when embryonic cells exit the pluripotent state.
2013-02-06 | GSE41256 | GEO
Project description:Post-translational modifications (PTMs) of histones exert fundamental roles in regulating gene expression. During development, groups of PTMs are constrained by unknown mechanisms into combinatorial patterns, which facilitate transitions from uncommitted embryonic cells into differentiated somatic cell lineages. Repressive histone modifications such as H3K9me3 or H3K27me3 have been investigated in detail, but the role of H4K20me3 in development is currently unknown. Here we show that Xenopus laevis Suv4-20h1 and h2 histone methyltransferases (HMTases) are essential for induction and differentiation of the neuroectoderm. Morpholino-mediated knockdown of the two HMTases leads to a selective and specific downregulation of genes controlling neural induction, thereby effectively blocking differentiation of the neuroectoderm. Global transcriptome analysis supports the notion that these effects arise from the transcriptional deregulation of specific genes rather than widespread, pleiotropic effects. Interestingly, morphant embryos fail to repress the Oct4-related Xenopus gene Oct-25. We validate Oct-25 as direct target of xSu4-20h enzyme-mediated gene repression, showing by chromatin immunoprecipitaton that it is decorated with the H4K20me3 mark downstream of the promoter in normal, but not in double-morphant, embryos. Since knockdown of Oct-25 protein significantly rescues the neural differentiation defect in xSuv4-20h double-morphant embryos, we conclude that the epistatic relationship between Suv4- 20h enzymes and Oct-25 controls the transit from pluripotent to differentiation-competent neural cells. Consistent with these results in Xenopus, murine Suv4-20h1/h2 double-knockout embryonic stem (DKO ES) cells exhibit increased Oct4 protein levels before and during EB formation, and reveal a compromised and biased capacity for in vitro differentiation, when compared to normal ES cells. Together, these results suggest a regulatory mechanism, conserved between amphibian and mammals, in which H4K20me3-dependent restriction of specific POU-V genes directs cell fate decisions, when embryonic cells exit the pluripotent state. Total RNA samples from Xenopus laevis embryos. Transcript levels were analyzed after injection of control or Suv420 morpholinos into blastomeres.
2013-02-06 | E-GEOD-41256 | biostudies-arrayexpress
Project description:Suv4-20h1/2 are histone methyltransferases that write the H4K20me2 and H4K20me3 marks. We knocked down these enzymes using translation blocking morpholinos in X. tropicalis animal caps and performed RNA-seq in order to investigate the impact of altering H4K20me state on epidermal differentiation. Knocking down Suv4-20h1/2 leads to a strong increase of H4K20me1 in bulk chromatin. To determine whether increased H4K20me1 is responsible for transcriptional changes in suv4-20h KD animal caps, we performed RNA-Seq for a rescue experiment with PHF8, an H4K20me1 demethylase.
2021-09-01 | GSE161248 | GEO
Project description:Suv4-20h1/2 are histone methyltransferases that write the H4K20me2 and H4K20me3 marks. We knocked down these enzymes using translation blocking morpholinos in X. tropicalis animal caps and performed RNA-seq in order to investigate the impact of altering H4K20me state on epidermal differentiation. Knocking down Suv4-20h1/2 leads to a strong increase of H4K20me1 in bulk chromatin. To determine whether increased H4K20me1 is responsible for transcriptional changes in suv4-20h KD animal caps, we performed RNA-Seq for a rescue experiment with PHF8, an H4K20me1 demethylase.
2021-09-01 | GSE161247 | GEO
Project description:Suv4-20h1/2 are histone methyltransferases that write the H4K20me2 and H4K20me3 marks. We knocked down these enzymes using translation blocking morpholinos in X. tropicalis animal caps and performed RNA-seq in order to investigate the impact of altering H4K20me state on epidermal differentiation. Knocking down Suv4-20h1/2 leads to a strong increase of H4K20me1 in bulk chromatin. To determine whether increased H4K20me1 is responsible for transcriptional changes in suv4-20h KD animal caps, we performed RNA-Seq for a rescue experiment with PHF8, an H4K20me1 demethylase.
2021-09-01 | GSE161250 | GEO
Project description:Suv4-20h1/2 are histone methyltransferases that write the H4K20me2 and H4K20me3 marks. We knocked down these enzymes using translation blocking morpholinos in X. tropicalis animal caps and performed RNA-seq in order to investigate the impact of altering H4K20me state on epidermal differentiation. Knocking down Suv4-20h1/2 leads to a strong increase of H4K20me1 in bulk chromatin. To determine whether increased H4K20me1 is responsible for transcriptional changes in suv4-20h KD animal caps, we performed RNA-Seq for a rescue experiment with PHF8, an H4K20me1 demethylase.
2021-09-01 | GSE161249 | GEO
Project description:Histone post-translational modifications (PTM) greatly influence gene expression and are widely considered to regulate progression through development. However, the function of some PTMs remain elusive. H4K20 is sequentially methylated in concert with the cell cycle. In proliferating cells, SET8/KTM5A writes the monomethyl mark in G2/M phase, which then is converted to the di- and trimethylated states by SUV4-20H1/H2 (KMT5B/KMT5C) methyltransferases in the next G1 and S phase. In quiescent, differentiated cells, H4K20me2 represents the most abundant histone modification present in vertebrate chromatin. To address the function of H4K20 methyl states in development, we blocked the deposition of H4K20me2 and H4K20me3 by depleting the SUV4-20H1 in Xenopus embryos. This results in a severe ciliogenic defect in multiciliated cells (MCCs), as well as the repression of hundreds of cytoskeleton and cilium related genes. Further, we demonstrate that this defect can be rescued by wildtype, but not catalytically inactive SUV4-20h1, as well as by overexpressing PHF8, an H4K20me1-specific histone demethylase. Ciliogenic defects cannot be rescued by master regulators of ciliogenesis on the phenotypic or transcriptional levels. Taken together, this indicates that SUV4-20H1 plays a critical role in multiciliogenesis.
2026-01-01 | GSE274390 | GEO
Project description:Histone post-translational modifications (PTM) greatly influence gene expression and are widely considered to regulate progression through development. However, the function of some PTMs remain elusive. H4K20 is sequentially methylated in concert with the cell cycle. In proliferating cells, SET8/KTM5A writes the monomethyl mark in G2/M phase, which then is converted to the di- and trimethylated states by SUV4-20H1/H2 (KMT5B/KMT5C) methyltransferases in the next G1 and S phase. In quiescent, differentiated cells, H4K20me2 represents the most abundant histone modification present in vertebrate chromatin. To address the function of H4K20 methyl states in development, we blocked the deposition of H4K20me2 and H4K20me3 by depleting the SUV4-20H1 in Xenopus embryos. This results in a severe ciliogenic defect in multiciliated cells (MCCs), as well as the repression of hundreds of cytoskeleton and cilium related genes. Further, we demonstrate that this defect can be rescued by wildtype, but not catalytically inactive SUV4-20h1, as well as by overexpressing PHF8, an H4K20me1-specific histone demethylase. Ciliogenic defects cannot be rescued by master regulators of ciliogenesis on the phenotypic or transcriptional levels. Taken together, this indicates that SUV4-20H1 plays a critical role in multiciliogenesis.
2026-01-01 | GSE274391 | GEO
Project description:Identification of genes regulated by XOct-25 overexpression in Xenopus ectoderm
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Project description:Comparative temporal analysis of wild-type Ptf1a, Neurog2 and mutant Ptf1a (Ptf1aW224A/W242A) overexpressing Xenopus explant transcriptomes after 6 and 25 hours of DEX induction.
| PRJNA342823 | ENA