Epigenetic regulation of cardiac myocyte cell cycle activity and growth.
We are seeking a talented postdoctoral scientist to investigate epigenetic mechanisms controlling cell cycle activity and growth of cardiac myocytes. This project will build on our recently published findings (Thienpont, Aronsen, Robinson et al., JCI 2017) and contribute to the development of new strategies for enhancing cardiac regeneration and ameliorate disease. Building on our recently published findings (Thienpont, Aronsen, Robinson et al., JCI 2017), we are analysing the contribution of the epigenome to determining and maintaining the post-mitotic state of the adult cardiac myocyte and how it can be manipulated to enhance regeneration and ameliorate disease. Given that the absence of proliferation is the Achilles' heel of the adult myocyte, underlying the inadequate proliferation required to repair the damaged heart, identifying how cardiac myocyte fate can be reprogrammed is an exciting and clinically relevant area of research. Moreover, the absence of proliferation in the adult heart provides an ideal substrate to examine epigenetic mechanisms independent of cell cycle.
The aim of this project is to probe the role of histone methylation in mediating the postnatal switch of the cardiac myocyte from hyperplastic growth to hypertrophic growth and in preventing/reversing deleterious hypertrophic remodelling associated with disease and ageing. NGS techniques including single cell approaches, will be used to examine whether certain populations of cardiac myocytes retain cell cycle activity in the adult and how cell cycle activity is altered post myocardial infarction. Small molecules and GM approaches will be used to manipulate expression/activity of enzymes responsible for modifying histone methylation. Human iPS derived cardiac myocytes will be used to complement animal studies. This research will test the notion that manipulation of histone methylation can be employed as a tool to reprogram cardiac myocyte phenotype,and excitingly enhance proliferation required for repair.
Genomic/epigenomic analysis is performed on cardiac myocytes isolated from genetically modified mice (cardiac specific knockout and transgenics, adeno-associated virus transduced), mouse models of disease (aortic banding, myocardial infarction), human tissue and iPS-derived cardiac myocytes.
We analyse transcriptomes and epigenomes, including methylomes of cell populations and single cells (next generation sequencing - ChIP-Seq/RNA-Seq/BS-Seq/single cell RNA-Seq).
As evidenced by our publications, we collaborate extensively within KU Leuven and outside to enhance our research.
If you are a talented scientist, with a special interest in working as part of a team to identify epigenetic mechanisms controlling cell fate transitions and disease processes in a biomedical context, please apply. It is also important that you have the ambition to dig deeper than the obvious and perform important research 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... For more information see https://icts.kuleuven.be/apps/jobsite/vacatures/54343960
This job comes from a partnership with Science Magazine and