Inhaltsverzeichnis
- 1 Wolf Reik
- 1.1 Epigenetic reprogramming in mammalian development
- 1.2 Latest publications
- 1.2.1 In vivo genome-wide profiling reveals a tissue-specific role for 5-formylcytosine.
- 1.2.2 Impairment of DNA Methylation Maintenance Is the Main Cause of Global Demethylation in Naive Embryonic Stem Cells.
- 1.2.3 Impairment of DNA Methylation Maintenance Is the Main Cause of Global Demethylation in Naive Embryonic Stem Cells.
Wolf Reik
The Babraham Institute, Cambridge, United Kingdom
Epigenetic reprogramming in mammalian development
Web Page
We are interested in epigenetic reprogramming in mammalian development, which occurs on a large scale in primordial germ cells and early embryos. Reprogramming probably has important roles in erasing parental imprints, returning the genome to a pluripotent state, removing acquired epimutations, and is potentially also important for the control of transposons. We are particularly interested in genome-wide erasure of DNA methylation, which may occur by a combination of mechanisms including passive demethylation, modification of methylcytosine by deamination or oxidation, and DNA repair. We are studying the dynamics of these novel DNA modifications by genome-wide profiling techniques during ES cell differentiation, and during experimental reprogramming to iPS cells. Some of the dynamics associated with early lineage decisions and reprogramming may lend themselves to computational and modeling approaches.
People involved in the lab:
- Tim Hore, postdoc
Related video to Wolf Reik:
Latest publications
In vivo genome-wide profiling reveals a tissue-specific role for 5-formylcytosine.
27356509 – 2016-07-01
Genome Biol 2016 Jun 29;17(1):141
Impairment of DNA Methylation Maintenance Is the Main Cause of Global Demethylation in Naive Embryonic Stem Cells.
27315559 – 2016-06-18
Mol Cell 2016 Jun 16;62(6):983
Impairment of DNA Methylation Maintenance Is the Main Cause of Global Demethylation in Naive Embryonic Stem Cells.
27237052 – 2016-05-31
Mol Cell 2016 Jun 16;62(6):848-61
View all their publications
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