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(A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular <t>smooth</t> <t>muscle</t> <t>cells</t> versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in <t>Human</t> <t>coronary</t> <t>artery</t> VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.
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(A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular <t>smooth</t> <t>muscle</t> <t>cells</t> versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in <t>Human</t> <t>coronary</t> <t>artery</t> VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.
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(A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular smooth muscle cells versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in Human coronary artery VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.

Journal: bioRxiv

Article Title: CAD variants act through ox-LDL-induced enhancer remodelling to alter VSMC gene programmes

doi: 10.64898/2026.04.21.718843

Figure Lengend Snippet: (A) AlphaGenome predicted quantile scores for prioritised CAD variants in vascular smooth muscle cells versus a non-vascular comparator (B cells) across chromatin and transcriptional output tracks. The quantile score represents a standardised rank of the impact of a variant, derived from quantile normalisation of the raw predicted score for each variant. (B) In-silico motif disruption analysis (motifbreakR) for prioritised variants within ABC enhancers, showing reference versus alternate PWM scores, coloured by ΔPWM (alternate − reference). TFs were restricted to those expressed in Human coronary artery VSMCs. (C) Locus-level example at rs9624456:CCTCA>T. Top left: AlphaGenome-predicted genome tracks comparing alternate versus reference alleles at rs9624456. Bottom left: observed genome tracks in Human coronary artery VSMCs following ox-LDL exposure. Top right: Hi-C contact map showing chromatin interactions within the SPECC1L-GUCD1 topologically associating domain (TAD). Bottom right: RNA-seq shows ox-LDL-associated induction of GUCD1 in Human coronary artery VSMCs. (D) CRISPR knockout (KO) experimental design and proliferation readout. Human coronary artery VSMCs were transfected with sgRNA, labelled with CFSE, and exposed to ox-LDL. CFSE histograms and quantification are shown; higher CFSE signal indicates reduced proliferation.

Article Snippet: Primary human coronary artery smooth muscle cells (Human coronary artery VSMCs) were obtained at passage 2 from Promocell (Heidelberg, Germany) and expanded before usage.

Techniques: Variant Assay, Derivative Assay, In Silico, Disruption, Hi-C, RNA Sequencing, CRISPR, Knock-Out, Transfection