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RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

ABSTRACT: RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

PROVIDER: PRJEB13071 | ENA |

REPOSITORIES: ENA

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RNA-seq of wild-type, Mbd3 and Sall4/1 mutant mouse embryonic stem cells

Project description:Mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors were cultured in self-renewing and neural differentiation conditions and profiled by RNA-seq.

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ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells

Project description:Members of the Nucleosome Remodeling and Deacetylase (NuRD) complex Mbd3 and Mi2beta (Chd4) along with pluripotency regulators Nanog, Oct4, Klf4 and Esrrb were profiled for chromatin association by ChIP-seq in mouse embryonic stem cells mutant for Mbd3, Sall4 and/or the related Sall1 pluripotency-associated factors.

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ChIP-seq of NuRD components and pluripotency factors in wild-type, Mbd3 and Sall4/1 mutant embryonic stem cells

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Project description:RNA-seq was performed for transcriptional analysis of wild-type mouse embryonic stem (ES) cells and an Mbd3 knockout line. Mbd3 is a core component of the Nucleosome Remodeling and Deacetylation (NuRD) complex, which modulates transcriptional heterogeneity and pluripotency gene expression in ES cells.

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Project description:Sall4 is a stem cell factor which is important for embryogenesis. We have genetically modified Sall4 in mouse embryonic stem cells to access the transcriptional changes. There are three different genetic modifications for the ES cells in the form of Sall4 Knockout (KO), Sall4 Zinc Finger Cluster 4 Mutation (ZFC4mut) and Sall4 Zinc Finger Cluster 1-2 Deletion (ZFC1-2Δ) respectively that we have considered for our study.

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Sall4: -/- NT1 vs TBV

Project description:Sall genes are expressed early in development and in diversity of embryonic and adult structures. Sall4 plays a crucial role during the development of a number of systems. Mutations in the SALL4 gene have been linked to Okihiro/acro-renal-ocular syndrome, in which patients exhibit forearm malformations and eye movement deficits. Homozygote and heterozygote Sall4 cells from mouse blastocysts were collected and used to design a genetrap mouse mutant line. The homozygote Sall4 ES cells form mouse blastocyst were hybridizised versus TBV wildtype cells to detect changes in gene expression. Three biological samples of different passages of the same clone of NT1 and TBV were analyzed in 13 chip hybridizations; each sample was analyzed in 2-5 experimental replicates including dye swap experiments. Keywords: others

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Expression profile of Sall4-null ES cells and Sall4 heterozygous ES cells

Project description:Sall4 is a mouse homolog of a causative gene of the autosomal dominant disorder known as Okihiro syndrome. We previously showed that Sall4 absence leads to lethality during peri-implantation and that Sall4-null embryonic stem (ES) cells proliferate poorly with intact pluripotency when cultured on feeder cells. However, a subsequent report indicated that shRNA-mediated Sall4 inhibition in ES cells led to a severe reduction in Oct3/4 and a secondary increase in Cdx2, which resulted in complete differentiation into the trophectoderm when cultured in the feeder-free condition. So we profiled gene expression changes when Sall4 is deleted in ES cells in the presence or absence of feeder cells. key word: embryonic stem (ES) cell, Sall4, feeder

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ChIP-Seq of ES-E14 mouse embryonic stem cells investigating changes in Sall4

Project description:Sall4 is a stem cell factor which is important for embryogenesis. We have genetically modified Sall4 in mouse embryonic stem cells to access the preference of Sall4 binding site. There are three different genetic modifications for the ES cells in the form of Sall4 Knockout (KO), Sall4 Zinc Finger Cluster 4 Mutation (ZFC4mut) and Sall4 Zinc Finger Cluster 1-2 Deletion (ZFC1-2Δ) respectively that we have considered for our study.

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Project description:Sall4 is a stem cell factor which is important for embryogenesis. We have genetically modified Sall4 in mouse embryonic stem cells to access the transcriptional changes. There are three different genetic modifications for the ES cells in the form of Sall4 Knockout (KO), Sall4 Zinc Finger Cluster 4 Mutation (ZFC4mut) and Sall4 Zinc Finger Cluster 4 Deletion (ZFC4Δ) respectively that we have considered for our study.

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