Figure 1. Gene expression analysis

Slides:

Advertisements

Similar presentations

Figure 3. (A) Effect of the ON length on the HTT mRNA knockdown efficiency. LNA/DNA CAG 10- to 19-mer PS ONs were transfected at 100 nM concentration into.

Advertisements

Figure 1. Schematic of the corA leader mRNA

Fig. 1. Significant clusters in the amygdala and dlPFC, four-way interaction effect (group by valence by temperature by time), small volume corrected.

Figure 1. Unified models predicting gene regulation based on landscapes of gene-regulating factors. For each gene, position specific combinatorial patterns.

Figure 1. srn_3610_sprC expression increases in the absence of SarA

Figure 5 ISOX and vorinostat partially restore splicing pattern in DM1 patient-derived fibroblasts. (A) ISOX and vorinostat partially rescue mis-splicing.

Figure 1. The scheme of RCAS

Figure 1. Overview of the Ritornello approach

Figure 1. AsCpf1 and LbCpf1-mediated gene editing in human cells

Figure 1. Annotation and characterization of genomic target of p63 in mouse keratinocytes (MK) based on ChIP-Seq. (A) Scatterplot representing high degree.

Fig. 1. — The life cycle of S. papillosus. (A) The life cycle of S

Figure 2. The graphic integration of CNAs with altered expression genes in lung AD and SCC. The red lines represent the amplification regions for CNA and.

From: Learning by Working in Big Cities

Fig. 1 Nodes in a conceptual knowledge graph

Figure 1: Pneumomediastinum and subcutaneous emphysema as indicated by the arrows. From: Pneumomediastinum and subcutaneous emphysema after successful.

From: DynaMIT: the dynamic motif integration toolkit

Figure 1. drb7.2 mutant plants display altered accumulation of endoIR-siRNA. Wild-type (Col-0) and drb7.2 mutant plants were subjected to high throughput.

From: Detection of Bacteriuria by Canine Olfaction

Figure 1. Stabilization of the hairpin structure by non-nucleotide linkers (-L-) following enzymatic circularization. Structures of the stilbene diether.

Figure 2. Force and concentration dependence of the rate at which ScTopA initiates DNA relaxation. (A) The initial time lag (ITL) for ScTopA activity displays.

Figure 4. (A) A schematic representation from constructs that include modifications in Flag-TDP-12xQ/N. TDP-12xQ/N F4/L (F147, 149, 229, 231/L); TDP-12xQ/N.

Figure 2. Ritornello captures the FLD from single-end sequencing data

Figure 1. The flow chart illustrates the construction process of anti-CRISPRdb, and the information that users can obtain from anti-CRISPRdb. From: Anti-CRISPRdb:

Figure 3. Schematic of the parameters to assess junctions in SpliceMap

Figure 1. Cdc48 is cotranscriptionally recruited on active genes

Figure 1. Loss of H2Bub1 promotes mutagenesis under conditions of replicative stress. (A) The graph shows the rates of spontaneous Canr mutation.

Figure 1. Workflow of the LISH assay. Step 1

Figure 1. Distinct chromatin regions isolated by the N-ChroP strategy

Figure 1. Effect of acute TNF treatment on transcription in human SGBS adipocytes as assessed by RNA-seq and RNAPII ChIP-seq. Following 10 days in vitro.

Figure 1. Complete work-flow of the Scasat

Figure 1. IGF2BP1 promotes SRF expression in cancer cells

Figure 2. Workflow of MethMotif Batch Query

From: Dynamic protein–RNA interactions in mediating splicing catalysis

Figure 1. (A) Number of 8-oxodGs per million of dGs (8-oxodg/106 dG) measured by LC-MS/MS in untreated (NT), UV-irradiated (UV) and NAC-treated.

Figure 3. Schematic representation of co-expression networks for BipA, SidD, and Erg11 encoding genes. Genes are represented by circles, with positive.

Figure 4. (A) Scatterplot of RPC4 T statistic (between TP0 and TP36) for the indicated groups of isolated tRNA genes (RPC4 peak only, n = 35; RPC4 + H3K4me3.

Figure 1. (A) The VEGF promoter PQS and scheme of G oxidation to OG, as well as (B) the proposed APE1-dependent pathway ... Figure 1. (A) The VEGF promoter.

Figure 1. A CRISPR/Cas9 synthetic lethal screen with PRMT5 inhibitor EPZ in H2171 cell line. (A) A pie chart ... Figure 1. A CRISPR/Cas9 synthetic.

Figure 1. Circular taxonomy tree based on the species that were sequenced in our study. Unless provided in the caption above, the following copyright applies.

Figure 1. A novel image analysis tool to monitor epigenetic changes in spatiotemporal distribution of chromatin in live ... Figure 1. A novel image analysis.

Figure 7. Primary cells from prostate tumours are more sensitive to ML than adjacent non-cancerous cells from the ... Figure 7. Primary cells from.

Figure 4. (A) Venn diagram showing the overlap of peaks differentially changed in DHT as compared to NT with peaks ... Figure 4. (A) Venn diagram showing.

Figure 1. AML containing the t(8:21) are extremely sensitive to CDK inhibitors. (A–C) Alamar blue assays were used to ... Figure 1. AML containing the.

Figure 1. Position and number of NLS improves genome editing by AsCas12a, LbCas12a and FnoCas12a. (A) General schematic ... Figure 1. Position and number.

Figure 1. BRCA1-associated R-Loop accumulation at a non-coding region upstream of ESR1 locus. (A) Alignment of DRIP-seq ... Figure 1. BRCA1-associated.

Figure 1. Schematic illustration of CSN and NDM construction and our statistic model. (A) CSN and NDM construction. (i) ... Figure 1. Schematic illustration.

Figure 1. Ratios of observed to expected numbers of exon boundaries aligning to boundaries of domain and disorder ... Figure 1. Ratios of observed to expected.

Figure 1. autoMLST workflow depicting placement and de novo mode

Figure 1. The 12 species in this study and details of the improved G4-seq method. (A) Phylogenetic representation of ... Figure 1. The 12 species in this.

Figure 1. Nanopore methylation calls are consistent with expected results and established technologies. (A) Metaplot of ... Figure 1. Nanopore methylation.

Point estimates with ... Point estimates with 95% CI. HR: hip replacement; KR: knee replacement. Unless provided in the caption above, the following copyright.

FIGURE 1 Participant flow diagram. Exercise Counseling Clinic (ECC).

Figure 1. Analysis of human TRIM5α protein with Blast-Search and PhyML+SMS ‘One click’ workflow. (A) NGPhylogeny.fr ... Figure 1. Analysis of human TRIM5α.

Alterations in mRNA 3′ UTR Isoform Abundance Accompany Gene Expression Changes in Human Huntington’s Disease Brains Lindsay Romo, Ami Ashar-Patel, Edith.

FIGURE 1 Study consort diagram

Figure 1. Illustration of DGR systems and their prediction using myDGR

Figure 1. Summary of experimental conditions and data normalization

Figure 1. Prediction result for birch pollen allergen Bet v 1 (PDB: 1bv1), as obtained by comparison to the cherry ... Figure 1. Prediction result for.

Figure 1. Using Voronoi tessellation to define contacts

Figure 1. PaintOmics 3 workflow diagram

Figure 1. Concept of poly(A) tail labeling for translation and localization analyses of reporter mRNAs. Azido-modified ... Figure 1. Concept of poly(A)

Figure 1. Accumulation kinetics of TC-NER factors reveal a CSA independent UVSSA recruitment. (A) Representative images ... Figure 1. Accumulation kinetics.

Fig. 1. —Synteny analysis of melon chromosome 1 (brown) and cucumber chromosome 7 (green) based on melon-cucumber ... Fig. 1. —Synteny analysis of melon.

Fig. 1. The ZNF804A interactome

Figure 1. 3C analysis of HEM3, BLM10, and SEN1 genes in rpb4Δ and isogenic wild type cells. (A) Schematic ... Figure 1. 3C analysis of HEM3, BLM10, and.

Figure 1. CSB does not affect the recruitment of OGG1 to oxidative DNA damage. (A) Representative stills of time-lapse ... Figure 1. CSB does not affect.

Figure 1. DNA-guided RNA cleavage activity

Figure 1 The workflow of CAR development from a hybridoma

Figure 1 Mechanisms of mitral regurgitation.

Figure 1. (A) Overview of ENPD including data source, data processing and features. Transcriptomes from TSA, genomes ... Figure 1. (A) Overview of ENPD.

Presentation transcript:

Figure 1. Gene expression analysis Figure 1. Gene expression analysis. (A) Barplot showing the number of differentially expressed genes in SMA-like mice at PND1 and PND5 in spinal cord, brain, liver and muscle. The number of down- and up-regulated genes is indicated below the barplot. (B) Venn diagrams of the overlap of significant genes in different tissues at PND1 and PND5. (C) Scatterplots of log2 fold-change estimates in spinal cord, brain, liver and muscle. Genes that were significant in both conditions are indicated in purple, genes that were significant only in the condition on the x axis are indicated in red, genes significant only in the condition on the y axis are indicated in blue. (D) Scatterplots of log2 fold-changes of genes in the indicated tissues that were statistically significantly different at PND1 versus the log<sub>2</sub> fold-changes at PND5. Genes that were also statistically significantly different at PND5 are indicated in red. The dashed grey line indicates a completely linear relationship, the blue line indicates the linear regression model based on the genes significant at PND1, and the red line indicates the linear regression model based on genes that were significant at both PND1 and PND5. Pearsons rho is indicated in black for all genes significant at PND1, and in red for genes significant at both time points. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 2. Expression of axon guidance genes is down-regulated in SMA-like mice at PND5 while stress genes are up-regulated. (A) Schematic depiction of the axon guidance pathway in mice from the KEGG database. Gene regulation is indicated by a color gradient going from down-regulated (blue) to up-regulated (red) with the extremity thresholds of log2 fold-changes set to −1.5 and 1.5, respectively. (B) qPCR validation of differentially expressed genes in SMA-like mice at PND5. (C) qPCR validation of differentially expressed genes in SMA-like mice at PND1. Error bars indicate SEM, n ≥ 3, **P-value < 0.01, *P-value < 0.05. White bars indicate heterozygous control mice, grey bars indicate SMA-like mice. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 3. Aberrant splicing with increased U2-intron retention in SMA-like mice. (A) Barplots showing the number of regions relative to the RefSeq annotation, either the total set of annotated regions, or those significantly alternatively spliced at PND1 or PND5 in the indicated tissues. (B) Venn diagram showing the overlap of genes with alternative splicing between tissues at PND5. (C) Volcano plots of exonic regions in spinal cord, brain, liver and muscle at PND5. Significantly differentially expressed regions overlapping known transcripts are indicated in red, novel significant regions are indicated in blue. Values exceeding chart limits are plotted at the corresponding edge and indicated by either up or downward facing triangle, or left/right facing arrow heads. Number of known and novel regions that are up or down-regulated are indicated in red (known) and blue (novel) in either the upper-left (down) or upper-right (up). (D) Piecharts of observed alternative splicing patterns in spinal cord, brain, liver and muscle at PND5 in either the full Cufflinks annotation or only the novel regions not overlapping previously annotated transcripts. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 4. U12-intron retention increases with disease progression Figure 4. U12-intron retention increases with disease progression. (A) Volcano plots of U12-intron retention SMA-like mice at PND1 in spinal cord, brain, liver and muscle. Significantly differentially expressed introns are indicated in red. Non-significant introns with foldchanges > 2 are indicated in blue. Values exceeding chart limits are plotted at the corresponding edge and indicated by either up or downward facing triangle, or left/right facing arrow heads. (B) Volcano plots of U12-intron retention in SMA-like mice at PND5 in spinal cord, brain, liver and muscle. Significantly differentially expressed introns are indicated in red. Non-significant introns with fold-changes >2 are indicated in blue. Values exceeding chart limits are plotted at the corresponding edge and indicated by either up or downward facing triangle, or left/right facing arrow heads. (C) Venn diagram of the overlap of common significant alternative U12-intron retention across tissue at PND1. (D) Venn diagram of the overlap of common significant alternative U12-intron retention across tissue at PND1. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 5. Increased U12-dependent intron retention in SMA mice Figure 5. Increased U12-dependent intron retention in SMA mice. (A) qPCR validation of U12-dependent intron retention at PND1 and PND5 in spinal cord. (B) qPCR validation of U12-dependent intron retention at PND1 and PND5 in brain. (C) qPCR validation of U12-dependent intron retention at PND1 and PND5 in liver. (D) qPCR validation of U12-dependent intron retention at PND1 and PND5 in muscle. Error bars indicate SEM, n ≥ 3, ***P-value < 0.001, **P-value < 0.01, *P-value < 0.05. White bars indicate heterozygous control mice, gray bars indicate SMA-like mice. Spl = spliced, Unspl = unspliced/retained intron. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 6. Knockdown of SMN in HeLa cells recapitulate the findings in SMA mice. (A) Western blot of SMN-targeting siRNA (SMN) versus non-targeting siRNA (NT) samples showing reduced expression of SMN protein. (B) Volcano-plot of U12-dependent intron retention in SMN-deficient HeLa cells. Significantly differentially retained introns are indicated in red. Non-significant introns with fold-changes >2 are indicated in blue. Values exceeding chart limits are plotted at the corresponding edge and indicated by upward facing triangle. (C) Venn diagram showing overlap of genes with U12-dependent intron retention in SMA mice at PND5 and SMN depleted HeLa cells. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 7. ASO treatment reverses the expression and splicing profiles of SMA. (A) ASO treatment increases inclusion of SMN2 exon 7. Inclusion percentage were estimated from RT-PCR product sizes quantitated on a fragment analyzer. (B) Scatter plot of log2 fold-changes of significant genes in spinal cord of ASO treated mice relative to saline treated SMA mice and log<sub>2</sub> fold-changes of the same genes in SMA mice relative to heterozygous controls. Genes that are significant in both comparisons are indicated in red and Pearson's correlation is indicated for these genes. (C) Heatmap of the average gene expression of genes in pathways significantly altered in the spinal cord of SMA mice relative to healthy controls. Gene expression values are derived from regularized log values and the normalized across samples setting the average to zero. (D) Barplot showing unadjusted P-values for the testing of reversal of the pathway in ASO treated mice relative to untreated SMA mice. (E) qPCR measurements of genes previously found to be deregulated in the spinal cord of SMA mice. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com

Figure 8. ASO treatment restores correct splicing of U12-dependent introns in SMA mice. (A) Volcano plots of U12-dependent introns in brain, spinal cord and liver of ASO treated SMA mice. Significantly differentially retained introns are indicated in red. Non-significant introns with fold-changes >2 are indicated in blue. Values exceeding chart limits are plotted at the corresponding edge and indicated by upward facing triangle. (B) Overlap of introns with significantly improved splicing in liver and spinal cord of ASO treated SMA mice. SMA = saline treated SMA mice, ASO = ASO treated SMA mice. (C) Overlap of introns significantly retained in SMA mice and introns significantly improved in ASO treated SMA mice in spinal cord and liver. (D) qPCR analysis of BAZ1B/Baz1b and MYO10/Myo10 U12-dependent intron splicing in HeLa SMN-KD samples, and spinal cord and liver in ASO treated SMA mice. From: RNA-sequencing of a mouse-model of spinal muscular atrophy reveals tissue-wide changes in splicing of U12-dependent introns Nucleic Acids Res. 2016;45(1):395-416. doi:10.1093/nar/gkw731 Nucleic Acids Res | © The Author(s) 2016. Published by Oxford University Press on behalf of Nucleic Acids Research.This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by-nc/4.0/), which permits non-commercial re-use, distribution, and reproduction in any medium, provided the original work is properly cited. For commercial re-use, please contact journals.permissions@oup.com