A Histone Mutant Reproduces the Phenotype Caused by Loss of Histone-Modifying Factor Polycomb
A Histone Mutant Reproduces the Phenotype Caused by Loss of Histone-Modifying Factor Polycomb
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DOI：
10.1126/science.1231382
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发表时间：
2013-02-08
期刊：
影响因子：
56.9
通讯作者：
Mueller, Juerg
中科院分区：
文献类型：
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作者：
Pengelly, Ana Raquel;Copur, Oemer;Mueller, Juerg
虽然许多后生动物的酶，添加或删除组蛋白的特定修饰是必不可少的转录调控因子，翻译后修饰组蛋白的功能意义还没有得到很好的理解。在这里，我们表明，在果蝇组蛋白H3（H3-K27）的赖氨酸27的点突变不能抑制转录的基因，通常被抑制的Polycomb抑制复合物2（PRC 2），甲基转移酶，修改H3-K27。此外，分化的H3-K27突变体细胞显示同源异型转化，如在PRC 2突变体细胞中所见。总之，这些分析表明，H3-K27是PRC 2修饰的Polycomb阻遏的关键生理底物。
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.