ELS effects on the epigenome

Early life stress (ELS) is associated with increased susceptibility for diseases in later life. Animal models and human studies suggest that this effect is mediated by epigenetic mechanisms. The problem is the inaccessibility of living brain tissue. So it is hard to determine whether ELS induced epigenetic changes in accessible peripheral cells. Furthermore, to answer the relationship between ELS, DNA methylation changes and adult phenotypes, we need a long time investigation of a human cohort from birth until adulthood.

We take a series of MeDIP genome-wide methylation analyses to explore the effects of ELS on genome-wide promoter methylation in human newborns. Several regions in MORC1 (MORC family CW-type zinc?nger 1) were differentially methylated in response to ELS in CD34+ cells and CD3+ T cells derived from the blood of human and monkey. In this study, we identi?ed 30 genes, whose methylation status was associated with ELS in all the tissues and species analyzed.

In monkey, a total of 1180 genes were differentially methylated. DNA methylation differences appeared soon after ELS exposure supporting the hypothesis that DNA methylation changes follow ELS, and go before the appearance of the clinical phenotypes later in life.

This study provides evidence for genome-wide and system-wide changes in DNA methylation in response to ELS.

Posttranslational modifications (PTMs) are key mechanisms used by both prokaryotes and eukaryotes to regulate protein activity. The small ubiquitin-like modifier (SUMO) is covalently linked to a variety of proteins and is important in regulation of protein stability. Isolation of SUMOylated proteins is challenging, for most SUMO substrates, only a small proportion of the total amount of protein (

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