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The BAF complex does not mediate GLI repression (WT Cut&RUN)

ABSTRACT: Purpose: This study seeks to identify SMARCC1-bound regions in the mouse limb. Methods: To identify SMARCC1 bound regions in the limb, we performed Cut&Run on pooled anterior and posterior wild-type forelimbs at E11.5 (43-44s; 3 replicates each) and on whole forelimb pairs at E9.5 (21-24s; 2 replicates). We identified 28,082 SMARCC1-bound regions in the anterior forelimb at E11.5, 42,530 regions in the E11.5 posterior limb, and 10,792 SMARCC1-bound regions at E9.5 (FDR<0.05). Results: We find that SMARCC1 is bound to most limb enhancer regions at late stages (E11.5). Additionally, We find that SMARCC1 is bound to the majority of HH-responsive GLI enhancers at E11.5 but only a small portion of GLI enhancers at E9.5.

ORGANISM(S): Mus musculus

PROVIDER: GSE224507 | GEO | 2024/02/03

REPOSITORIES: GEO

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The BAF complex does not mediate GLI repression (Gli3 null Cut&RUN)

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The BAF complex does not mediate GLI repression (ATAC-Seq)

Project description:Purpose: This study seeks to determine whether Smarcc1 mediates GLI repression through chromatin compaction in the limb. Methods: To determine if Smarcc1 mediated GLI repression through chormatin compaction, we used genomic approached to determine changes in chromatin accessibility in control and Smarcc1-conditional mutants. We performed ATAC-seq on individually genotyped anterior forelimbs at E11.5 (40-48s) on control (2 replicates) and PrxCre/+;Smarcc1c/c (3 replicates) embryos. From this experiment we identified ~10,000 differentially accessible regions (FDR<0.05). Results: We find that SMARCC1 is required to maintain chromatin accessibility at thousands of regions within the mouse limb, including most HH-responsive GLI enhancers

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Genome-wide maps of chromatin accessibility in response to Hh signaling in mouse embryonic forelimb buds

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2020-01-21 | GSE107877 | GEO

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Project description:Development of the complex structure of the vertebrate limb requires carefully orchestrated interactions between multiple regulatory pathways and proteins. Among these, precise regulation of 5’ Hox transcription factor expression is essential for proper limb bud patterning and development. Here, we identified Geminin (Gmnn) as a novel regulator of this process. A conditional model of Gmnn deficiency resulted in loss or severe reduction of forelimb skeletal elements, while both the forelimb autopod and hindlimb were unaffected. 5’ Hox gene expression expanded into more proximal and anterior regions of embryonic forelimb buds in this Gmnn-deficient model. A second conditional model of Gmnn deficiency instead caused a similar but less severe reduction of hindlimb skeletal elements and hindlimb polydactyly, while not affecting the forelimb. An ectopic posterior Shh signaling center was evident in the anterior hindlimb bud of Gmnn-deficient embryos in this model. This center ectopically expressed Hoxd13, the Hoxd13 target Shh, and the Shh target Ptch1, while these mutant hindlimb buds also had reduced levels of the cleaved, repressor form of Gli3, a Shh pathway antagonist. Together, this work delineates a new role for Gmnn in modulating Hox expression to pattern the vertebrate limb.

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Genome wide maps of chromatin modification in response to Hh signaling in mouse embryonic forelimb buds

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