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10X Genomics 10x scatac seq library v2 kit
(A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by <t>10X</t> 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.
10x Scatac Seq Library V2 Kit, supplied by 10X Genomics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/scatac+seq+libraries/bio_rxiv__64898__2026__04__18__719392-227-7-12?v=10X+Genomics
Average 86 stars, based on 1 article reviews
10x scatac seq library v2 kit - by Bioz Stars, 2026-08
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1) Product Images from "Systematic identification of chromatin organizers as tuners of intratumoral heterogeneity"

Article Title: Systematic identification of chromatin organizers as tuners of intratumoral heterogeneity

Journal: bioRxiv

doi: 10.64898/2026.04.18.719392

(A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by 10X 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.
Figure Legend Snippet: (A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by 10X 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.

Techniques Used: Transduction, In Vivo, Genome Wide, Control, Two Tailed Test, Expressing

(A) Experimental schematic. RNF8 and MIS18A CRISPRi/a MDA-MB-231 lines were hash-pooled and pro-filed by 10X scATAC-seq. (B) Genome-wide open-chromatin CV change per genomic locus upon CRISPRi or CRISPRa perturbation of RNF8 and MIS18A. Accessibility was filtered for gene regions; a value of zero indicates no change relative to non-targeting control. P -values by two-sided Wilcoxon signed-rank test. (C, D) Left: binarized open/closed chromatin scores (ArchR) across cells (rows) and genomic position (columns) for representative loci. Yellow boxes highlight reduced accessibility dispersion upon knockdown (C) and increased dispersion upon overexpression (D) . Right: CV for the highlighted locus in each perturbation condition. P -values by Fisher’s exact test.
Figure Legend Snippet: (A) Experimental schematic. RNF8 and MIS18A CRISPRi/a MDA-MB-231 lines were hash-pooled and pro-filed by 10X scATAC-seq. (B) Genome-wide open-chromatin CV change per genomic locus upon CRISPRi or CRISPRa perturbation of RNF8 and MIS18A. Accessibility was filtered for gene regions; a value of zero indicates no change relative to non-targeting control. P -values by two-sided Wilcoxon signed-rank test. (C, D) Left: binarized open/closed chromatin scores (ArchR) across cells (rows) and genomic position (columns) for representative loci. Yellow boxes highlight reduced accessibility dispersion upon knockdown (C) and increased dispersion upon overexpression (D) . Right: CV for the highlighted locus in each perturbation condition. P -values by Fisher’s exact test.

Techniques Used: Genome Wide, Control, Dispersion, Knockdown, Over Expression



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10X Genomics 10x scatac seq library v2 kit
(A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by <t>10X</t> 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.
10x Scatac Seq Library V2 Kit, supplied by 10X Genomics, used in various techniques. Bioz Stars score: 86/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/scatac+seq+libraries/bio_rxiv__64898__2026__04__18__719392-227-7-12?v=10X+Genomics
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
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A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung <t>tissue</t> <t>scATAC-seq</t> data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.
Scatac Seq Libraries, supplied by 10X Genomics, used in various techniques. Bioz Stars score: 90/100, based on 1 PubMed citations. ZERO BIAS - scores, article reviews, protocol conditions and more
https://www.bioz.com/product/scatac+seq+libraries/pmc11188612-109-1-11?v=10X+Genomics
Average 90 stars, based on 1 article reviews
scatac-seq libraries - by Bioz Stars, 2026-08
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(A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by 10X 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.

Journal: bioRxiv

Article Title: Systematic identification of chromatin organizers as tuners of intratumoral heterogeneity

doi: 10.64898/2026.04.18.719392

Figure Lengend Snippet: (A) Schematic of the Perturb-seq workflow. MDA-MB-231 cells were transduced with CRISPRi or CRISPRa sgRNAs targeting the 16 in vivo -validated COs, followed by 10X 3 ′ scRNA-seq. Genome-wide CV was computed for each perturbation and compared to size-matched random control groupings. (B) Mean and standard error of mean barplots for genome-wide CV change upon CRISPRi (left) or CRISPRa (right) perturbation of RNF8 and MIS18A. A value of 1 indicates no change relative to non-targeting control. P -values by one-sample two-tailed Student’s t -test ( μ = 1). (C, D) Per-gene transcript CV in CRISPRi cells versus non-targeting controls for RNF8 (C) and MIS18A (D) . Each horizontal line represents a gene; P -values by two-sided paired Student’s t -test. Percentages indicate proportion of genes that decrease (top) or increase (bottom) in CV relative to non-targeting control. (E) CV analysis in an independent patient tumor scRNA-seq cohort . Patients were stratified into quartiles by RNF8 or MIS18A expression ( n = 4 per quartile). P -values by two-sided Wilcoxon signed-rank test.

Article Snippet: For scATAC-seq library generation, we used the 10X scATAC-seq library v2 kit (10X Genomics, PN-1000390).

Techniques: Transduction, In Vivo, Genome Wide, Control, Two Tailed Test, Expressing

(A) Experimental schematic. RNF8 and MIS18A CRISPRi/a MDA-MB-231 lines were hash-pooled and pro-filed by 10X scATAC-seq. (B) Genome-wide open-chromatin CV change per genomic locus upon CRISPRi or CRISPRa perturbation of RNF8 and MIS18A. Accessibility was filtered for gene regions; a value of zero indicates no change relative to non-targeting control. P -values by two-sided Wilcoxon signed-rank test. (C, D) Left: binarized open/closed chromatin scores (ArchR) across cells (rows) and genomic position (columns) for representative loci. Yellow boxes highlight reduced accessibility dispersion upon knockdown (C) and increased dispersion upon overexpression (D) . Right: CV for the highlighted locus in each perturbation condition. P -values by Fisher’s exact test.

Journal: bioRxiv

Article Title: Systematic identification of chromatin organizers as tuners of intratumoral heterogeneity

doi: 10.64898/2026.04.18.719392

Figure Lengend Snippet: (A) Experimental schematic. RNF8 and MIS18A CRISPRi/a MDA-MB-231 lines were hash-pooled and pro-filed by 10X scATAC-seq. (B) Genome-wide open-chromatin CV change per genomic locus upon CRISPRi or CRISPRa perturbation of RNF8 and MIS18A. Accessibility was filtered for gene regions; a value of zero indicates no change relative to non-targeting control. P -values by two-sided Wilcoxon signed-rank test. (C, D) Left: binarized open/closed chromatin scores (ArchR) across cells (rows) and genomic position (columns) for representative loci. Yellow boxes highlight reduced accessibility dispersion upon knockdown (C) and increased dispersion upon overexpression (D) . Right: CV for the highlighted locus in each perturbation condition. P -values by Fisher’s exact test.

Article Snippet: For scATAC-seq library generation, we used the 10X scATAC-seq library v2 kit (10X Genomics, PN-1000390).

Techniques: Genome Wide, Control, Dispersion, Knockdown, Over Expression

A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung tissue scATAC-seq data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis

doi: 10.1038/s41467-026-70193-w

Figure Lengend Snippet: A Schematic diagram of the SiO 2 mouse model. Mice were divided into control (saline, n = 3) and experimental (SiO 2 , n = 3) groups by tracheal injection. After 20 weeks, mice were euthanized, and lung single-cell suspensions were prepared for sequencing. B Validation of the SiO 2 mouse model. H&E and Masson staining showed increased inflammation and fibrosis in the lungs of SiO 2 treated mice ( n = 3 mice per group). C UMAP plots of lung tissue scRNA-seq data from SiO 2 -induced and control mice. D UMAP plots of lung tissue scATAC-seq data from SiO 2 -induced and control mice. E Violin plots showed expression of marker genes of scRNA-seq data from SiO 2 -induced and control mice. F In scATAC-seq data from SiO 2 -induced and control mice, peaks for marker genes were identified for each subcelltype. G The UMAP plot showed endothelial subpopulations in scRNA-seq data from SiO 2 -induced and control mice. UMAP plot ( H ) and violin plot ( I ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 784 cells) and control ( n = 816 cells) mice. J The UMAP plot showed the endothelial subpopulations of scATAC-seq data. UMAP plot ( K ) and violin plot ( L ) showed the MS scores of endothelial cells in scRNA-seq data of Silica-induced ( n = 387 cells) and control ( n = 689 cells) mice. M GO enrichment analysis of motifs showed that signaling pathways associated with mechanical stress were enriched in ECs. Statistical significance of GO terms was calculated using the hypergeometric test. N Table showing TF motifs of endothelial cells enriched in mechanical stress-related pathways by scATAC-seq data. P values were calculated using the hypergeometric test. I, L: Violin plot displayed the mean (yellow diamond) the median (center line), the interquartile range, and the whiskers (1.5 × interquartile range). P value was calculated using the two-tailed unpaired t-test. Source data are provided as a Source Data file.

Article Snippet: We collected single-cell suspensions from lung tissues to prepare scRNA-seq and scATAC-seq libraries using 10X Genomics kits to measure RNA and chromatin accessibility (Fig. ).

Techniques: Control, Saline, Injection, Single Cell, Sequencing, Biomarker Discovery, Staining, Expressing, Marker, Protein-Protein interactions, Two Tailed Test

A BLM intratracheal model scheme (n = 3 per group). B H&E and Masson validation of inflammation/fibrosis (n = 3 per group). C Lung scRNA-seq UMAP. D scATAC-seq UMAP subclusters. E Venn showing Piezo1 and Piezo2 as co-regulated genes across silica and BLM bulk, scRNA-seq and scATAC-seq data. F scATAC-seq coverage peaks of Piezo1 and Piezo2 . G CD31 and CD45-sorted EC bulk-RNA-seq heatmap and bar chart (n = 3 per group). Gene expression levels were Z-score normalized. P values were calculated using the two-tailed unpaired t-test. H PIEZO1 (green) and Ve-cad (red) co-staining and quantification in fibrotic mouse lungs (n = 4). UMAP and bar charts (mean ± SEM) of PIEZO1 + ( I ) and PIEZO2 + ( J ) EC counts in normal controls (n = 5) versus IPF (n = 4) patients. P values were calculated using the two-tailed unpaired t-test. K PIEZO1 (green) and CD31 (red) co-staining and quantification in human IPF vs normal lungs (n = 10). L Meta-analysis of five GEO datasets showing elevated PIEZO1 in IPF ECs. Standardized mean difference (SMD) were calculated as Hedges’ g with corresponding 95% confidence intervals. Data were shown as mean ± SEM, H and K: two-tailed unpaired t-tests, Source data are provided as a Source Data file.

Journal: Nature Communications

Article Title: Single-cell multiomics uncovers an endothelial mechanosensitive PIEZO1-IL-33 axis driving pulmonary fibrosis

doi: 10.1038/s41467-026-70193-w

Figure Lengend Snippet: A BLM intratracheal model scheme (n = 3 per group). B H&E and Masson validation of inflammation/fibrosis (n = 3 per group). C Lung scRNA-seq UMAP. D scATAC-seq UMAP subclusters. E Venn showing Piezo1 and Piezo2 as co-regulated genes across silica and BLM bulk, scRNA-seq and scATAC-seq data. F scATAC-seq coverage peaks of Piezo1 and Piezo2 . G CD31 and CD45-sorted EC bulk-RNA-seq heatmap and bar chart (n = 3 per group). Gene expression levels were Z-score normalized. P values were calculated using the two-tailed unpaired t-test. H PIEZO1 (green) and Ve-cad (red) co-staining and quantification in fibrotic mouse lungs (n = 4). UMAP and bar charts (mean ± SEM) of PIEZO1 + ( I ) and PIEZO2 + ( J ) EC counts in normal controls (n = 5) versus IPF (n = 4) patients. P values were calculated using the two-tailed unpaired t-test. K PIEZO1 (green) and CD31 (red) co-staining and quantification in human IPF vs normal lungs (n = 10). L Meta-analysis of five GEO datasets showing elevated PIEZO1 in IPF ECs. Standardized mean difference (SMD) were calculated as Hedges’ g with corresponding 95% confidence intervals. Data were shown as mean ± SEM, H and K: two-tailed unpaired t-tests, Source data are provided as a Source Data file.

Article Snippet: We collected single-cell suspensions from lung tissues to prepare scRNA-seq and scATAC-seq libraries using 10X Genomics kits to measure RNA and chromatin accessibility (Fig. ).

Techniques: Biomarker Discovery, RNA Sequencing, Gene Expression, Two Tailed Test, Staining