Influence of post-translational modifications on the biology of linker histone HIS-24 in Caenorhabditis elegans

• Applicant: Dr. Monika Jedrusik-Bode
• Subject Area: General Genetics and Functional Genome Biology
• Term: from 2006 to 2012
• Project identifier: Deutsche Forschungsgemeinschaft (DFG) - Project number 19228257

Epigenetic modifications play an important role in the regulation of chromatin structure and transcription. The H3-K9 and H3-K27 methylation cause transcriptional silencing and H3-K4 methylation has been linked to transcriptional activation. These modifications influence the transitions between the open and compacted chromatin states. The Polycomb Repressive Group Complexes (PRC) with histone-lysine methyltransferase (HMT) unit are responsible for the lysine-K9 and -K27 methylation. In human tissue cells and in in vitro experiments the PRC complexes methylate core histone H3-K27 and linker histone H1-K26 dependent on histone deacetylase SirT1 (VAQUERO et al., 2004; KUZMICHEV et al., 2005). In C. elegans the methylation of core histones H3-K4, -K9, -K27 is regulated in the germline by cytoplasmic linker histone H1.1 (JEDRUSIK and SCHULZE, 2005; submitted to Development). H1.1 plays an important role in the function of HMT in the germline and specifically enhances the deficiency of H3-K27 methylation in the mes-mutant animals. In addition, the absence of SIR-2 protein has influence on the methylation of H3-K9 and the mis-localization of H1.1 in the germ nuclei in C. elegans (JEDRUSIK and SCHULZE, unpublished observation). Our understanding of the influence of core histones and linker histone methylation on the organization of higher order chromatin structure and function will be advanced by the identification of the HMT(s), the gene targets and interaction partners of histone methylation in invertebrates C. elegans.

• DFG Programme: Research Grants
• Host: Professor Dr. Wolfgang Fischle