We are seeking a talented bioinformatician to apply their expertise to investigate epigenetic mechanisms controlling cardiac myocyte phenotype and fate choices in postnatal development, disease and ageing. This project will leverage recent data generated in the laboratory and build on our recently published findings (Thienpont, Aronsen, Robinson et al., JCI 2017) contributing to the development of new strategies to target cardiovascular disease. Building on our recently published findings(Thienpont, Aronsen, Robinson et al., JCI 2017), this project aims to dissect thecontribution of the epigenome to determining and maintaining the post-mitotic stateof the adult cardiac myocyte and how it can be manipulated to amelioratedisease. Given that the absence of proliferation is the Achilles’ heel of theadult myocyte, underlying the inadequate proliferation required to repair thedamaged heart, identifying how cardiac myocyte fate can be reprogrammed is anexciting and clinically relevant area of research. Moreover, the absence ofproliferation in the adult heart provides an ideal substrate to examineepigenetic mechanisms independent of cell cycle.
This project will probe the role of theepigenome in postnatal development of the adult cardiac myocyte and howdegradation of the epigenetic landscape contributes to cardiac remodelling indisease and ageing. In this regard, the contribution of cellular heterogeneity tocardiac phenotype will also be investigated by single cell approaches. Throughthese analysis, nodal regulators and networks will be identified and theircontribution to disease/cardiac myocyte phenotype tested in in vivo models andin patient samples. This research will also contribute to identification ofstrategies (key targets) to manipulate the epigenome to reprogram cardiacmyocyte phenotype to the healthy adult state.
Genomic/epigenomic analysis is performed on cardiacmyocytes isolated from genetically modified mice (cardiac specific knockout andtransgenics, adeno-associated virus transduced), mouse models of disease(aortic banding, myocardial infarction), human tissue and iPS-derived cardiacmyocytes. We analyse transcriptomes and epigenomes, including methylomes ofcell populations and single cells (next generation sequencing – ChIP-Seq/RNA-Seq/BS-Seq/singlecell RNA-Seq). As evidenced by our publications, we collaborate extensivelywithin KU Leuven and outside to advance our research.
Your role: If you are a talented scientist,with a special interest in working as part of a team to identify epigeneticmechanisms controlling cell fate transitions and disease processes in abiomedical context, please apply. You will work closely with bench scientistsin the laboratory and in addition to your own project, you will haveopportunities to collaborate on other related projects. It is also importantthat you have the ambition to dig deeper than the obvious and perform importantresearch that is relevant to human disease mechanisms.
Thienpont, B., J.M. Aronsen, E.L. Robinson, H.Okkenhaug, E. Loche, A. Ferrini, P. Brien, K. Alkass, A. Tomasso, A. Agrawal,O. Bergmann, I. Sjaastad, W. Reik, and H.L. Roderick. 2017. The H3K9dimethyltransferases EHMT1/2 protect against … For more information see https://icts.kuleuven.be/apps/jobsite/vacatures/54343852
This job comes from a partnership with Science Magazine and