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The nucleosome remodeler SNF2L modulates WNT signaling for cellular homeostasis

ABSTRACT: 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.

ORGANISM(S): Homo sapiens

PROVIDER: GSE30471 | GEO | 2012/05/11

SECONDARY ACCESSION(S): PRJNA143489

REPOSITORIES: GEO

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The nucleosome remodeler SNF2L modulates WNT signaling for cellular homeostasis

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

The Chromatin Remodelling Contributions of Snf2l in Cerebellar Granule Neuron Differentiation [ATAC-Seq]

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 | GSE122172 | GEO

The Chromatin Remodelling Contributions of Snf2l in Cerebellar Granule Neuron Differentiation [RNA-Seq]

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The ISWI ATPase Snf2L is required for superovulation and regulates Fgl2 in differentiating mouse granulosa cells

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

2013-05-01 | GSE42997 | GEO

The ISWI ATPase Snf2L is required for superovulation and regulates Fgl2 in differentiating mouse granulosa cells

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Mouse E15.5 cortices: Snf2l Ex6 deleted mice versus wild type controls

Project description:Gene expression profiling of mouse cortices in which the experimental strain lacks Exon 6 of the Snf2l gene which encodes an ATP-binding motif that is critical for chromatin re-modeling Comparison of gene expression in E15.5 cortices of Snf2l-Ex6DEL mice versus wild type controls. Two samples of each strain were used, with one pair of samples utilized for two of the replicates (dye-flip), the second pair then used for the third replicate.

2012-04-09 | E-GEOD-34998 | biostudies-arrayexpress

Mouse E15.5 cortices: Snf2l Ex6 deleted mice versus wild type controls

2012-04-10 | GSE34998 | GEO

Mammalian ISWI and SWI/SNF selectively mediate binding of distinct groups of transcription factors (MNase-seq data sets)

Project description:Remodelers define nucleosome composition, presence and position. Mammalian imitation-switch-type (ISWI) comprise one class, mostly relying on the ATPase Snf2h for activity. We show that embryonic stem cells are viable without Snf2h, enabling to study its function and contrast it to Brg1, the ATPase of SWI/SNF. Loss of Snf2h specifically affects nucleosomal positioning and increases linker lengths genome-wide providing in vivo evidence for ISWI function in ruling nucleosomal spacing. Systematic analysis of transcription factor binding reveals selective requirement on either remodeling activity. One group, containing the transcriptional repressor REST depend on BRG1, while a non-overlapping set including the insulator protein CTCF, relies on Snf2h. Importantly localized reduction in CTCF binding decreases long-range interactions. Collectively, this links mammalian ISWI to nuclear organization, demonstrates its cellular role for nucleosomal periodicity and reveals that transcription factors rely on specific remodeling pathways for proper genomic binding.

2019-04-18 | GSE112134 | GEO

Mammalian ISWI and SWI/SNF selectively mediate binding of distinct groups of transcription factors (ChIP-seq data sets)

2019-04-18 | GSE112132 | GEO