Senior researcher or postdoc in the lab of computational neurobiology

at  Universiteit Antwerpen

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LET’S SHAPE THE FUTURE - UNIVERSITY OF ANTWERP

The University of Antwerp is a dynamic, forward-thinking, European university. We offer an innovative academic education to more than 20000 students, conduct pioneering scientific research and play an important service-providing role in society. We are one of the largest, most international and most innovative employers in the region. With more than 6000 employees from 100 different countries, we are helping to build tomorrow’s world every day. Through top scientific research, we push back boundaries and set a course for the future – a future that you can help to shape.
The VIB Center for Molecular Neurology at The University of Antwerp is looking for a full-time (100%) senior researcher/postdoc in the lab of computational neurobiology

POSITION

In the Computational Neurobiology lab, we study causal mechanisms underlying normal and aberrant cellular decision-making in the human brain in health and neurodegenerative diseases. We investigate the role of spatial chromatin organization in cell fate acquisition and maintenance, using a variety of targeted and genome-wide profiling technologies and develop statistical and machine learning approaches for multimodal data integration and cis-regulatory network reconstruction.
We are looking for a talented and highly motivated scientist for a postdoctoral position in our lab to work on a project at the intersection genetics, systems biology and computational biology to study the regulatory mechanisms underlying cell-type specific switching of alternative gene isoform in different types of dementia, generously supported by the Alzheimer’s Association.
The human brain shows some of the widest isoform diversity of any organ and has therefore been an important model for studying alternative splicing. Intriguingly, recent studies showed widespread changes in isoform usage, specifically in usage of alternative transcription start site (ATSS) and alternative transcription termination site (ATTS) of causal disease genes, in Alzheimer’s disease (AD), Parkinson’s disease (PD) and Dementia with Lewy Bodies (DLB). These observations to the forefront the significance of ATTS/ATTS choice across neurodegenerative diseases and the need for comprehensive holistic research into the mechanisms regulating it, as currently the knowledge of these mechanisms is severely lacking. Most recently, large-scale changes in 3D chromatin organization and epigenetic factors have been shown to affect or correlate with alternative splicing/exon usage. Yet, there has never been a systematic study of the precise mechanisms governing ATSS/ATTS choice, on a genome-wide scale at high-resolution, nor of the role of the combined action of chromatin organization and epigenetic factors in these mechanisms. The proposed project is aiming to bridge this gap, (i) build isoform-specific regulatory atlas for the human brain in health and disease, (ii) identify causal regulatory elements and transcription factors responsible for determining ATSS and ATTS choice in disease and (ii) identify putative causal disease isoforms with a genetic underpinning in dementia.

Please refer the Job description for details