Imperial College London
Alternate

Professor Dame Amanda Fisher

Faculty of Medicine, Institute of Clinical Sciences

Visiting Professor
 
 
 
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Contact

 

amanda.fisher

 
 
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Assistant

 

Ms Alessandra Lisini +44 (0)20 3313 8236

 
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Location

 

CRB (Clinical Research Building)Hammersmith Campus

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Summary

 

Publications

Citation

BibTex format

@article{Van:2017:10.1016/j.celrep.2017.01.010,
author = {Van, de Pette M and Abbas, A and Feytout, A and McNamara, G and Bruno, L and To, WK and Dimond, A and Sardini, A and Webster, Z and McGinty, J and Paul, EJ and Ungless, MA and French, PMW and Withers, DJ and Uren, A and Ferguson-Smith, AC and Merkenschlager, M and John, RM and Fisher, AG},
doi = {10.1016/j.celrep.2017.01.010},
journal = {Cell Reports},
pages = {1090--1099},
title = {Visualizing changes in Cdkn1c expression links early life adversity to imprint mis-regulation in adults},
url = {http://dx.doi.org/10.1016/j.celrep.2017.01.010},
volume = {31},
year = {2017}
}
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RIS format (EndNote, RefMan)

TY  - JOUR
AB  - Imprinted genes are regulated according to parental origin and can influence embryonic growth and metabolism and confer disease susceptibility.Here we designed sensitive allele-specific reporters to non-invasively monitor imprinted Cdkn1cexpression  in  mice  and  showed  that  expression  was  modulated  by environmental  factors  encounteredin  utero.Acute  exposure  to chromatin modifyingdrugs  resulted  in  de-repression  of  paternally  inherited  (silent) Cdkn1calleles  in  embryos  that  was  temporary and  resolved  after  birth.In contrast,  deprivation  of  maternal  dietary  proteinin uteroprovoked permanent de-repression   of   imprinted Cdkn1cexpression   that   was   sustained   into adulthood  and  occurred  through  a  folate-dependent  mechanism  of  DNA methylation loss.Given the function of imprinted genes in regulating behavior and   metabolic   processes   in   adults,   these   results   establish   imprinting deregulation  as  a  credible  mechanism  linking  early  life  adversity  to  later-life outcomes.Furthermore,Cdkn1c-luciferasemice  offer  non-invasivetools  to identify  factors  that  disrupt  epigenetic  processes  and  strategies  to  limit  their long-term impact.
AU  - Van,de Pette M
AU  - Abbas,A
AU  - Feytout,A
AU  - McNamara,G
AU  - Bruno,L
AU  - To,WK
AU  - Dimond,A
AU  - Sardini,A
AU  - Webster,Z
AU  - McGinty,J
AU  - Paul,EJ
AU  - Ungless,MA
AU  - French,PMW
AU  - Withers,DJ
AU  - Uren,A
AU  - Ferguson-Smith,AC
AU  - Merkenschlager,M
AU  - John,RM
AU  - Fisher,AG
DO  - 10.1016/j.celrep.2017.01.010
EP  - 1099
PY  - 2017///
SN  - 2211-1247
SP  - 1090
TI  - Visualizing changes in Cdkn1c expression links early life adversity to imprint mis-regulation in adults
T2  - Cell Reports
UR  - http://dx.doi.org/10.1016/j.celrep.2017.01.010
UR  - https://www.sciencedirect.com/science/article/pii/S2211124717300281?via%3Dihub
UR  - http://hdl.handle.net/10044/1/43828
VL  - 31
ER  -
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