The Origin

“It is much more important to know what sort of a patient has a disease than what sort of a disease a patient has.”

---Sir William Osler---

Showing posts with label Stability of Epigenetic Modifications. Show all posts
Showing posts with label Stability of Epigenetic Modifications. Show all posts

Friday, August 1, 2008

Stability and flexibility of epigenetic gene regulation in mammalian development.

Nature. 2007 May 24;447(7143):425-32.
Stability and flexibility of epigenetic gene regulation in mammalian development.
Reik W.
Laboratory of Developmental Genetics and Imprinting, The Babraham Institute, Cambridge CB22 3AT, UK. wolf.reik@bbsrc.ac.uk
During development, cells start in a pluripotent state, from which they can differentiate into many cell types, and progressively develop a narrower potential. Their gene-expression programmes become more defined, restricted and, potentially, 'locked in'. Pluripotent stem cells express genes that encode a set of core transcription factors, while genes that are required later in development are repressed by histone marks, which confer short-term, and therefore flexible, epigenetic silencing. By contrast, the methylation of DNA confers long-term epigenetic silencing of particular sequences--transposons, imprinted genes and pluripotency-associated genes--in somatic cells. Long-term silencing can be reprogrammed by demethylation of DNA, and this process might involve DNA repair. It is not known whether any of the epigenetic marks has a primary role in determining cell and lineage commitment during development.
PMID: 17522676 [PubMed - indexed for MEDLINE]


Link for Full Text: http://www.nature.com/nature/journal/v447/n7143/full/nature05918.html