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The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.

Cuadrado A, Remeseiro S, Graña O, Pisano DG, Losada A - Nucleic Acids Res. (2015)

Bottom Line: More than one third of cohesin binding sites differ between the two tissues and these show reduced overlap with CCCTC-binding factor (CTCF) and are enriched at the regulatory regions of tissue-specific genes.Analyses of chromatin contacts at the Protocadherin (Pcdh) and Regenerating islet-derived (Reg) gene clusters, mostly expressed in brain and pancreas, respectively, revealed remarkable differences that correlate with the presence of cohesin.We could not detect significant changes in the chromatin contacts at the Pcdh locus when comparing brains from wild-type and SA1 embryos.

View Article: PubMed Central - PubMed

Affiliation: Chromosome Dynamics Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Melchor Fernández Almagro 3, 28029 Madrid, Spain.

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Cohesin is enriched at the promoters of actively transcribed genes. (A) Transcriptional profiles from the cortex (left) and pancreas (right) of 10-week-old mice were determined by RNA-seq. Tissue-specific genes were selected for each tissue (see main text for details) and further confirmed by Gene Ontology analysis. (B) Cohesin distribution around the TSS (±6 kb) of genes expressed specifically in cortex (upper panels) and pancreas (lower panels) defined as peak frequency (%). Both SMC1 and SA1 distributions are shown. (C) Gene expression changes between wild-type and SA1  brains (KO) from E17.5 embryos were characterized by RNA-seq (FDR < 0.05). (D) Cohesin distribution around the TSS of genes found to be down-regulated (left) and up-regulated (right) in SA1  embryonic brains.
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Figure 2: Cohesin is enriched at the promoters of actively transcribed genes. (A) Transcriptional profiles from the cortex (left) and pancreas (right) of 10-week-old mice were determined by RNA-seq. Tissue-specific genes were selected for each tissue (see main text for details) and further confirmed by Gene Ontology analysis. (B) Cohesin distribution around the TSS (±6 kb) of genes expressed specifically in cortex (upper panels) and pancreas (lower panels) defined as peak frequency (%). Both SMC1 and SA1 distributions are shown. (C) Gene expression changes between wild-type and SA1 brains (KO) from E17.5 embryos were characterized by RNA-seq (FDR < 0.05). (D) Cohesin distribution around the TSS of genes found to be down-regulated (left) and up-regulated (right) in SA1 embryonic brains.

Mentions: We next analysed cohesin distribution around the transcription start site (TSS) of the genes that are expressed specifically in each tissue. To assess tissue-specific gene expression RNA-seq was performed in the same samples used for ChIP (Supplementary Tables S2 and S3). We defined tissue-specific genes as those differentially expressed when compared with the other tissue (log2FC > 4, FDR < 0.05), in which the expression should be low, i.e. Fragments Per Kilobase of exon per Million fragments mapped (FPKM) <3. Using these criteria, we selected 2126 cortex-specific genes and 514 pancreas-specific genes. Gene ontology analyses verified the functional specificity of the gene sets (Figure 2A and Supplementary Table S4). We found that cohesin binding sites (both SMC1 and SA1) are enriched around the TSS of tissue-specific genes mainly in the tissue in which they are expressed (Figure 2B).


The contribution of cohesin-SA1 to gene expression and chromatin architecture in two murine tissues.

Cuadrado A, Remeseiro S, Graña O, Pisano DG, Losada A - Nucleic Acids Res. (2015)

Cohesin is enriched at the promoters of actively transcribed genes. (A) Transcriptional profiles from the cortex (left) and pancreas (right) of 10-week-old mice were determined by RNA-seq. Tissue-specific genes were selected for each tissue (see main text for details) and further confirmed by Gene Ontology analysis. (B) Cohesin distribution around the TSS (±6 kb) of genes expressed specifically in cortex (upper panels) and pancreas (lower panels) defined as peak frequency (%). Both SMC1 and SA1 distributions are shown. (C) Gene expression changes between wild-type and SA1  brains (KO) from E17.5 embryos were characterized by RNA-seq (FDR < 0.05). (D) Cohesin distribution around the TSS of genes found to be down-regulated (left) and up-regulated (right) in SA1  embryonic brains.
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Related In: Results  -  Collection

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Figure 2: Cohesin is enriched at the promoters of actively transcribed genes. (A) Transcriptional profiles from the cortex (left) and pancreas (right) of 10-week-old mice were determined by RNA-seq. Tissue-specific genes were selected for each tissue (see main text for details) and further confirmed by Gene Ontology analysis. (B) Cohesin distribution around the TSS (±6 kb) of genes expressed specifically in cortex (upper panels) and pancreas (lower panels) defined as peak frequency (%). Both SMC1 and SA1 distributions are shown. (C) Gene expression changes between wild-type and SA1 brains (KO) from E17.5 embryos were characterized by RNA-seq (FDR < 0.05). (D) Cohesin distribution around the TSS of genes found to be down-regulated (left) and up-regulated (right) in SA1 embryonic brains.
Mentions: We next analysed cohesin distribution around the transcription start site (TSS) of the genes that are expressed specifically in each tissue. To assess tissue-specific gene expression RNA-seq was performed in the same samples used for ChIP (Supplementary Tables S2 and S3). We defined tissue-specific genes as those differentially expressed when compared with the other tissue (log2FC > 4, FDR < 0.05), in which the expression should be low, i.e. Fragments Per Kilobase of exon per Million fragments mapped (FPKM) <3. Using these criteria, we selected 2126 cortex-specific genes and 514 pancreas-specific genes. Gene ontology analyses verified the functional specificity of the gene sets (Figure 2A and Supplementary Table S4). We found that cohesin binding sites (both SMC1 and SA1) are enriched around the TSS of tissue-specific genes mainly in the tissue in which they are expressed (Figure 2B).

Bottom Line: More than one third of cohesin binding sites differ between the two tissues and these show reduced overlap with CCCTC-binding factor (CTCF) and are enriched at the regulatory regions of tissue-specific genes.Analyses of chromatin contacts at the Protocadherin (Pcdh) and Regenerating islet-derived (Reg) gene clusters, mostly expressed in brain and pancreas, respectively, revealed remarkable differences that correlate with the presence of cohesin.We could not detect significant changes in the chromatin contacts at the Pcdh locus when comparing brains from wild-type and SA1 embryos.

View Article: PubMed Central - PubMed

Affiliation: Chromosome Dynamics Group, Molecular Oncology Programme, Spanish National Cancer Research Centre (CNIO), Melchor Fernández Almagro 3, 28029 Madrid, Spain.

Show MeSH
Related in: MedlinePlus