A Histone Mutant Reproduces the Phenotype Caused by Loss of Histone-Modifying Factor Polycomb

Author:

Pengelly Ana Raquel1,Copur Ömer1,Jäckle Herbert2,Herzig Alf2,Müller Jürg1

Affiliation:

1. Chromatin and Chromosome Biology Research Group, Max Planck Institute of Biochemistry, Am Klopferspitz 18, 82152 Martinsried, Germany.

2. Department of Molecular Developmental Biology, Max Planck Institute for Biophysical Chemistry, Am Fassberg 11, 37077 Göttingen, Germany.

Abstract

Genetic Epigenetics Posttranslational modifications of histone proteins have been implicated in the regulation of gene transcription in organisms ranging from yeast to humans. However, epigenetic regulators can modify multiple proteins. By mutating specific histone sites in Drosophila , Pengelly et al. (p. 698 ) demonstrate that mutation of lysine 27 of histone H3 causes the same transcriptional defects as those observed in mutants lacking the methyltransferase PRC2 that modifies this H3 residue. These results demonstrate the functional importance of H3-K27 methylation in Polycomb repression. Furthermore, this genetic approach may be applied to investigating numerous other metazoan-specific histone modifications.

Publisher

American Association for the Advancement of Science (AAAS)

Subject

Multidisciplinary

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