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

被引：230

作者：

Pengelly, Ana Raquel ^{[1
]}

Copur, Oemer ^{[1
]}

Jaeckle, Herbert ^{[2
]}

Herzig, Alf ^{[2
]}

Mueller, Juerg ^{[1
]}

机构：

[1] Max Planck Inst Biochem, Chromatin & Chromosome Biol Res Grp, D-82152 Martinsried, Germany

[2] Max Planck Inst Biophys Chem, Dept Mol Dev Biol, D-37077 Gottingen, Germany

来源：

SCIENCE | 2013年 / 339卷 / 6120期

关键词：

METHYLATION; MECHANISMS;

D O I：

10.1126/science.1231382

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Although many metazoan enzymes that add or remove specific modifications on histone proteins are essential transcriptional regulators, the functional significance of posttranslational modifications on histone proteins is not well understood. Here, we show in Drosophila that a point mutation in lysine 27 of histone H3 (H3-K27) fails to repress transcription of genes that are normally repressed by Polycomb repressive complex 2 (PRC2), the methyltransferase that modifies H3-K27. Moreover, differentiated H3-K27 mutant cells show homeotic transformations like those seen in PRC2 mutant cells. Taken together, these analyses demonstrate that H3-K27 is the crucial physiological substrate that PRC2 modifies for Polycomb repression.

引用

页码：698 / 699

页数：2

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