Project Summary
Recent data on the transcriptional cofactor AF9 and the histone 3 (H3) methyltransferase DOT1L suggest an association of H3 di- and trimethylation at lysine 79 (H3K79me2/3) with the neurodegenerative disease ataxia. We will provide novel insights in H3K79me2/3 function through analyses of CAG repeat length variations of the human AF9 gene in ataxia patients and controls, and through investigation of the phenotype of Dot1l-deficient mice with regard to cerebellar function. Perspectively, we will identify and interfere with epigenetically regulated risk factors associated with specific neural dysfunctions.
Project-relevant publications
- Roidl D., Hellbach N., Bovio P., Villarreal A., Heidrich S., Nestel S., Gruning B., Bonisch U. and Vogel T. (2015) DOT1L activity promotes proliferation and protects cortical neural stem cells from activation of ATF4-DDIT3-mediated ER stress in vitro. Stem Cells
- Backofen R. and Vogel T. (2014) Biological and bioinformatical approaches to study crosstalk of long-non-coding RNAs and chromatin-modifying proteins. Cell Tissue Res 356, 507-526.
- Vogel T. and Lassmann S. (2014) Epigenetics: development, dynamics and disease. Cell Tissue Res 356, 451-455.
