Oxford Events, the new replacement for OxTalks, will launch on 16th March. From now until the launch of Oxford Events, new events cannot be published or edited on OxTalks while all existing records are migrated to the new platform. The existing OxTalks site will remain available to view during this period.
From 16th, Oxford Events will launch on a new website: events.ox.ac.uk, and event submissions will resume. You will need a Halo login to submit events. Full details are available on the Staff Gateway.
For our next talk, in the BDI/CHG (gen)omics Seminar series, we will be hearing Emilie Wigdor, Postdoctoral Research Scientist, The Sanders Group and Dr Narjes Rohani, Postdoctoral Research Associate. The Sanders and Rinaldi labs. We’re delighted to host Emilie and Narges in what promises to be a great talk!
Date: Tuesday 17 March 2026
Time: 9:30 – 10:30 am
Location: BDI/OxPop Seminar room 0
Talk title: Cellular and Developmental Context of Genetic Risk in Brain Disorders, Dr Narjes Rohani
Talk title: Cell-type-specific regulatory dysregulation in autism, Emilie Wigdor
Bio: Dr Narjes Rohani is a postdoctoral research associate in the Sanders and Rinaldi labs, where she investigates the genetic and epigenetic mechanisms underlying neurodevelopmental and psychiatric disorders. Her work integrates multi-omic data, including bulk and single-cell RNA sequencing, single-cell chromatin accessibility, and bulk DNA sequencing, from brain tissues across developmental stages to understand when and how these conditions emerge. Ultimately, she aims to identify regulatory enhancers that may serve as potential therapeutic targets.
Abstract: Although thousands of GWAS variants for brain disorders have been identified, it remains unclear when and where in the brain these genetic effects are most active. To address this gap, we integrated GWAS data for a range of brain disorders with cell type– and developmental stage–specific ATAC-seq and RNA-seq data using stratified LD score regression and gene expression enrichment analyses. We identified the developmentally specific neuronal and non-neuronal cell populations in which genetic risk is concentrated. Our results reveal strong enrichment of psychiatric risk in postnatal excitatory neurons and distinct microglial contributions to neurodegenerative diseases. Finally, we identified an enhancer element that may serve as a potential therapeutic target for SOX5 haploinsufficient syndrome, demonstrating how single-cell and developmental stage–specific data can nominate biologically meaningful and clinically relevant regulatory regions.
Bio:
Dr Emilie Wigdor is a postdoctoral researcher in the Sanders Lab, where she integrates whole-genome sequencing with single-nucleus RNA and ATAC sequencing to investigate the regulatory basis of neurodevelopmental and psychiatric disorders. Her research focuses on how common and rare genetic variation converge on cell-type-specific molecular pathways in autism.
She completed her PhD at the Wellcome Sanger Institute, studying the contribution of common variation to rare neurodevelopmental disorders and the impact of spliceosomal gene variants. Her work has also examined sex differences in autism, including genetic and epidemiological evidence supporting a female protective effect. Dr Wigdor previously held a Junior Research Fellowship at the Centre for Personalised Medicine at St Anne’s College.
Abstract:
Autism is highly phenotypically and genetically heterogeneous, raising the question of whether diverse aetiologies converge on shared regulatory programs. Using paired single-nucleus RNA and ATAC sequencing from postmortem human cortex, including cases with and without identified pathogenic variants, we mapped transcriptional and chromatin accessibility changes at cell-type resolution.
Dysregulation was concentrated in excitatory and inhibitory neurons and was most pronounced among genetically diagnosed cases, yet genome-wide effect sizes were partially concordant with cases without a known genetic diagnosis. Integration of chromatin accessibility data identified recurrent increases in RFX family motif accessibility across neuronal populations. RFX3, an established autism risk gene identified through rare variant studies, showed coordinated changes in motif accessibility and expression, and was associated with altered immediate-early gene programs, implicating activity-dependent regulatory pathways.
Together, these findings suggest that diverse genetic aetiologies converge on common neuronal regulatory pathways revealed by integrated single-nucleus profiling.
————————————————————————————————————————
All members of the University are welcome to join, please let reception at BDI know you’re here for the seminar and sign-in. We hope you can join us!
We also now have a mailing list –
To be added, ping genomics_bdi_whg-subscribe@maillist.ox.ac.uk (with any message), you should get a bounce-back with three options to confirm your subscription. Follow any of those options, and with a bit of luck you should be signed up!
As a reminder, the (gen)omics seminar series runs every other Tuesday morning and is intended to increase interaction between individuals working in genomics across Oxford. We encourage in-person attendance where possible. There is time for discussion over, tea, coffee and pastries after the talks.
Hybrid Option:
Please note that these meetings are closed meetings and only open to members of the University of Oxford to encourage sharing of new and unpublished data. Please respect our speakers and do not share the link with anyone outside of the university.
Microsoft Teams meeting
teams.microsoft.com/meet/34860831816590?p=6hPeBaocoVaZWTWAlm
Meeting ID: 348 608 318 165 90
Passcode: WR2NA22f
