The chromatin remodeling ATPases SNF2H and SNF2L position nucleosomes adjacent to CTCF and other transcription factors.
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ABSTRACT:
REPOSITORIES: ENA
Dataset's files
| Action | DRS | |||
|---|---|---|---|---|
| ERR1299110_1.fastq.gz | Fastqsanger.gz | |||
| ERR1299110_2.fastq.gz | Fastqsanger.gz | |||
| ERR1299120_1.fastq.gz | Fastqsanger.gz | |||
| ERR1299120_2.fastq.gz | Fastqsanger.gz | |||
| ERR1299130_1.fastq.gz | Fastqsanger.gz |
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Project description:ISWI is an evolutionary conserved ATPase that catalyzes nucleosome remodeling in several different complexes. Two mammalian ISWI orthologs, SNF2H and SNF2L, have specialized functions despite their high similarity. Due to the lack of reagents the functions of SN2L in human cells had not been established. Newly established specific monoclonal antibodies and selective RNA interference protocols now enabled a comprehensive characterization of loss-of-function phenotypes in human cells. Contrasting earlier results obtained in the mouse model, we found SNF2L broadly expressed in primary human tissues. Depletion of SNF2L in HeLa cells led to enhanced proliferation, morphological alterations and increased migration. These phenomena were explained by transcriptome profiling, which identified SNF2L as a modulator of the Wnt signaling network. The cumulative effects of SNF2L depletion on gene expression portray the cell in a state of activated Wnt signaling characterized by increased proliferation and chemotactic locomotion. High levels of SNF2L expression in normal melanocytes contrast to undetectable expression in malignant melanoma. In summary, our data document an anti-correlation between SNF2L expression and several features characteristic of malignant cells. Total RNA samples from human HeLa cells. Transcript levels were analyzed after luciferase, SNF2H and SNF2L RNAi.
2012-05-10 | E-GEOD-30471 | biostudies-arrayexpress
Project description:Snf2l and the closely related protein, Snf2h, play a critical role in embryonic and post-natal brain development. Murine models lacking functional Snf2h or Snf2l point to complementary activities of these remodelers; Snf2h cKO mice present with a significantly reduced cerebellum, while Snf2l Ex6DEL cerebella are larger than their wild-type counterparts. Granule neuron progenitors (GNPs) isolated from Ex6DEL cerebella display delayed cell cycle exit and hindered terminal differentiation compared to wild-type littermates. Moreover, loss of Snf2l activity results in widespread transcriptome shifts which underlie the Ex6DEL GNP differentiation phenotype. In particular, key transcription factors (TFs) are differentially expressed without Snf2l remodelling activity. We confirm that ERK pathway activation is misregulated in Ex6DEL GNPs, possibly in response to elevated fibroblast growth factor 8 (Fgf8) expression in these cultures. We find that Snf2l activity maintains the chromatin landscape throughout GNP differentiation, as Ex6DEL cultures have a global increase in chromatin accessibility. We suggest that Snf2l-mediated chromatin condensation is responsible for proper regulation of gene expression programs in GNP differentiation.
2019-12-31 | GSE122173 | GEO
Project description:Snf2l and the closely related protein, Snf2h, play a critical role in embryonic and post-natal brain development. Murine models lacking functional Snf2h or Snf2l point to complementary activities of these remodelers; Snf2h cKO mice present with a significantly reduced cerebellum, while Snf2l Ex6DEL cerebella are larger than their wild-type counterparts. Granule neuron progenitors (GNPs) isolated from Ex6DEL cerebella display delayed cell cycle exit and hindered terminal differentiation compared to wild-type littermates. Moreover, loss of Snf2l activity results in widespread transcriptome shifts which underlie the Ex6DEL GNP differentiation phenotype. In particular, key transcription factors (TFs) are differentially expressed without Snf2l remodelling activity. We confirm that ERK pathway activation is misregulated in Ex6DEL GNPs, possibly in response to elevated fibroblast growth factor 8 (Fgf8) expression in these cultures. We find that Snf2l activity maintains the chromatin landscape throughout GNP differentiation, as Ex6DEL cultures have a global increase in chromatin accessibility. We suggest that Snf2l-mediated chromatin condensation is responsible for proper regulation of gene expression programs in GNP differentiation.
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Project description:ISWI is an evolutionary conserved ATPase that catalyzes nucleosome remodeling in several different complexes. Two mammalian ISWI orthologs, SNF2H and SNF2L, have specialized functions despite their high similarity. Due to the lack of reagents the functions of SN2L in human cells had not been established. Newly established specific monoclonal antibodies and selective RNA interference protocols now enabled a comprehensive characterization of loss-of-function phenotypes in human cells. Contrasting earlier results obtained in the mouse model, we found SNF2L broadly expressed in primary human tissues. Depletion of SNF2L in HeLa cells led to enhanced proliferation, morphological alterations and increased migration. These phenomena were explained by transcriptome profiling, which identified SNF2L as a modulator of the Wnt signaling network. The cumulative effects of SNF2L depletion on gene expression portray the cell in a state of activated Wnt signaling characterized by increased proliferation and chemotactic locomotion. High levels of SNF2L expression in normal melanocytes contrast to undetectable expression in malignant melanoma. In summary, our data document an anti-correlation between SNF2L expression and several features characteristic of malignant cells.
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Project description:Within the genomes of metazoans, nucleosomes are highly organised adjacent to the binding sites for a subset of transcription factors. Here we have sought to investigate which chromatin remodelling enzymes are responsible for this. We find that the ATP-dependent chromatin remodelling enzyme SNF2H plays a major role organising arrays of nucleosomes adjacent to the binding sites for the architectural transcription factor CTCF sites and acts to promote CTCF binding. At many other factor binding sites SNF2H and the related enzyme SNF2L contribute to nucleosome organisation. The action of SNF2H at CTCF sites is functionally important as depletion of CTCF or SNF2H affects transcription of a common group of genes. This suggests that chromatin remodelling ATPase's most closely related to the Drosophila ISWI protein contribute to the function of many human gene regulatory elements.
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Project description:Nucleosome remodeling factors regulate the occupancy and positioning of nucleosomes genome-wide through ATP-driven DNA translocation. While many nucleosomes are well- and consistently positioned, some nucleosomes and nucleosome-like structures are more sensitive to nuclease digestion or transitory in nature. To better understand the role of nucleosome remodeling factors in generating and clearing these alternative nucleosome structures, we depleted murine embryonic stem cells of the remodeler ATPases BRG1 and SNF2H then performed MNase-seq in murine embryonic stem cells. We performed MNase-seq under high- and low-MNase conditions to assess the effects of nucleosome remodeling factors on nuclease-sensitive or “fragile” nucleosome occupancy. In parallel, we gel-extracted MNase-digested fragments to enrich for another alternative nucleosome structure, the overlapping dinucleosome. Overlapping dinucleosomes are composed of two canonical nucleosomes, asymmetrically lacking one H2A:H2B dimer and wrapped by ~250 bp of DNA. In vitro studies of nucleosome remodeling have suggested that the collision of adjacent nucleosomes by nucleosome sliding can stimulate formation of overlapping dinucleosomes. Using these methods, we were able to identify fragile nucleosomes and overlapping dinucleosomes near transcription start sites and gene-distal DNaseI hypersensitive sites in mouse embryonic stem cells, among other loci. We find that BRG1 consistently stimulates occupancy of fragile nucleosomes but represses occupancy of overlapping dinucleosomes through its nucleosome remodeling function, while SNF2H expression slightly increases fragile nucleosome occupancy.
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Project description:We investigate the role of Snf2l in ovaries by characterizing a mouse bearing an inactivating deletion on the ATPase domain of Snf2l (Ex6DEL). Snf2l mutant mice produce significantly fewer eggs than control mice when superovulated. Thus, gonadotropin stimulation leads to a significant deficit in secondary follicles and an increase in abnormal antral follicles. We profiled the expression of granulosa cells from Snf2l WT and Ex6DEL mice treated with pregnant mares' serum gonadotropin followed by human chorionic gonadotropin
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Project description:We investigate the role of Snf2l in ovaries by characterizing a mouse bearing an inactivating deletion on the ATPase domain of Snf2l (Ex6DEL). Snf2l mutant mice produce significantly fewer eggs than control mice when superovulated. Thus, gonadotropin stimulation leads to a significant deficit in secondary follicles and an increase in abnormal antral follicles. We profiled the expression of granulosa cells from Snf2l WT and Ex6DEL mice treated with pregnant mares' serum gonadotropin followed by human chorionic gonadotropin Granulosa cells from either Snf2l WT or Ex6DEL mice treated with PMSG followed by hCG were collected at 0h and 4h post-hCG. Each array includes granulosa cells pooled from 5 mice.
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