Neural Regeneration Research ›› 2018, Vol. 13 ›› Issue (7): 1191-1192.doi: 10.4103/1673-5374.235029

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Histone methylation in Huntington’s disease: are bivalent promoters the critical targets?

Nóra Zsindely, László Bodai   

  1. Department of Biochemistry and Molecular Biology, University of Szeged,Szeged, Hungary
  • Received:2018-05-08 Online:2018-07-15 Published:2018-07-15
  • Contact: László Bodai, Ph.D., bodai@bio.u-szeged.hu.
  • Supported by:

    This work was supported by Hungarian National Research, Development and Innovation Office (NKFIH) grants K-112294, GINOP-2.3.2-15-2016-00032 and GINOP-2.3.2-15-2016-00034 to LB.

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Abstract:

Huntington’s disease (HD) is a currently incurable, late onset, progressive,ultimately fatal neurological disorder (Bates et al., 2015). We have recently published the results of comprehensive genetic interaction tests aimed at identification of histone methyltransferases and demethylases involved in HD pathogenesis in a Drosophila model of the disease.The methylation state of histone proteins regulates the accessibility of chromatin structure by which it may influence transcriptional dysregulation observed in HD. We found that several factors affecting the methylation state of histone H3 lysine 4 (H3K4) and H3K27 residues influenced HD symptoms and identified the H3K27 specific demethylase, Utx, as a druggable target whose inhibition ameliorated neurodegeneration.These results in combination with previous findings suggest that bivalent chromatin regions, which are characterized by simultaneous presence of activating trimethylated-H3K4 (H3K4me3) and repressing H3K27me3 chromatin marks, might play a prominent role in HD pathogenesis.