Underlying mechanisms of re-programingreproduction following early life adversity
A high burden of inflammatory diseasewas correlated with later puberty onset and earlier menopause in a study ofmigrant women, possibly suggesting an adaptive response to optimizereproductive success. We combined data from that human study with anappropriate mouse model to investigate the molecular mechanisms involved inthis response. We found altered DNA methylation and expression levels ofseveral genes in reproductive tissues, and showed direct effects of thesealterations on reproductive function. Understanding the molecular eventsinduced by early-life stress and identification these stable epigenetic marksmight be used to help assess a woman’s reproductive status and predict the length of herreproductive lifespan.
Time: Tuesday, March 16, 2022, 13:00pm.
Place: Hybrid- in the Faculty Auditorium /
