Imperial College London

ProfessorMichaelSchneider

Faculty of MedicineNational Heart & Lung Institute

Chair in Cardiology
 
 
 
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Contact

 

+44 (0)013 34621727m.d.schneider Website

 
 
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Location

 

ICTEM buildingHammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Fujita:2017:10.1016/j.celrep.2017.10.036,
author = {Fujita, J and Freire, P and Coarfa, C and Benham, AL and Gunaratne, P and Schneider, MD and Dejosez, M and Zwaka, TP},
doi = {10.1016/j.celrep.2017.10.036},
journal = {Cell Reports},
pages = {1562--1573},
title = {Ronin Governs Early Heart Development by Controlling Core Gene Expression Programs.},
url = {http://dx.doi.org/10.1016/j.celrep.2017.10.036},
volume = {21},
year = {2017}
}

RIS format (EndNote, RefMan)

TY  - JOUR
AB - Ronin (THAP11), a DNA-binding protein that evolved from a primordial DNA transposon by molecular domestication, recognizes a hyperconserved promoter sequence to control developmentally and metabolically essential genes in pluripotent stem cells. However, it remains unclear whether Ronin or related THAP proteins perform similar functions in development. Here, we present evidence that Ronin functions within the nascent heart as it arises from the mesoderm and forms a four-chambered organ. We show that Ronin is vital for cardiogenesis during midgestation by controlling a set of critical genes. The activity of Ronin coincided with the recruitment of its cofactor, Hcf-1, and the elevation of H3K4me3 levels at specific target genes, suggesting the involvement of an epigenetic mechanism. On the strength of these findings, we propose that Ronin activity during cardiogenesis offers a template to understand how important gene programs are sustained across different cell types within a developing organ such as the heart.
AU - Fujita,J
AU - Freire,P
AU - Coarfa,C
AU - Benham,AL
AU - Gunaratne,P
AU - Schneider,MD
AU - Dejosez,M
AU - Zwaka,TP
DO - 10.1016/j.celrep.2017.10.036
EP - 1573
PY - 2017///
SN - 2211-1247
SP - 1562
TI - Ronin Governs Early Heart Development by Controlling Core Gene Expression Programs.
T2 - Cell Reports
UR - http://dx.doi.org/10.1016/j.celrep.2017.10.036
UR - http://hdl.handle.net/10044/1/53399
VL - 21
ER -