Ian Richard Jones

The paper uses CRISPR-based functional genomics to identify noncoding regulatory elements and variants affecting schizophrenia-associated gene expression.

The paper identifies combinatorial TF-cRE interactions in mouse basal ganglia development, revealing modules that drive GABAergic neurogenesis and suppress other fates.

The paper identifies PRC2.1's role in opposing G1 progression by regulating CCND1 and CCND2, showing its importance in cell proliferation across multiple cancer types.

The paper identifies functional CREs in iPSCs and neurons and links them to neuropsychiatric disease risk variants.

The paper identifies a transcription factor network and enhancers involved in cortical regional patterning using mouse embryonic data.

This paper develops a transcriptome-based polygenic risk score (T-PRS) linking depression-related cortical gene expression changes to brain morphology and symptom severity in MDD.

CRISPRpath enables parallel characterization of cis-regulatory elements for multiple genes in a pathway, identifying functional enhancers and distinguishing their impact on gene expression.

The paper reports exome sequencing findings in bipolar disorder, identifying AKAP11 as a shared risk gene with schizophrenia through ultra-rare protein-truncating variants.

This study characterizes 3D epigenomic landscapes during human corticogenesis, revealing chromatin looping and super interactive promoters involved in lineage-specific gene regulation.

This study identifies traits associated with polygenic risk for depression using UK Biobank data and finds causal links between depression risk and brain structure, as well as environmental interactions.

This study investigates whether genetic variation in the Major Histocompatibility Complex (MHC) is associated with depression risk, finding no significant associations at a conservative threshold.

The paper identifies cis-regulatory chromatin contacts in neural cells and links them to genetic variants associated with complex neurological disorders.

This study investigates genetic associations between major depression and cardio-metabolic traits, finding shared genetic aetiology regardless of depression onset age.

This study finds that genetic risk scores for insomnia and sleep duration differ between bipolar I and II subtypes, suggesting distinct genetic liabilities.

This study shows that adult microglia self-renew to restore homeostasis after ablation, with specific maturation programs and spatial organization.

The study finds that rare copy number variants (CNVs) contribute to bipolar disorder risk primarily in schizoaffective disorder bipolar type cases, with differences in CNV burden and schizophrenia polygenic risk scores between subtypes.

This study conducts the largest GWAS for PTSD, identifying 6 genome-wide significant loci in European and African ancestries and highlighting novel biological pathways.

The paper applies polygenic risk scoring to a large family with bipolar and depressive disorders to study genetic risk patterns and anticipation.

The paper investigates the role of rare copy number variants (CNVs) in depression, finding that neurodevelopmental CNVs are associated with increased depression risk.

This paper validates EHR-based BD phenotyping algorithms by showing their genetic correlation with traditional BD cases, suggesting they identify genetically similar cases.

The paper investigates the relationship between polygenic risk scores for schizophrenia and psychotic features in bipolar disorder, finding a gradient of genetic liability based on the level of mood-incongruent symptoms.