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

Pengelly A. R., Copur Ö. U., Jaeckle H., Herzig A., Mueller J.

SCIENCE, cilt.339, sa.6120, ss.698-699, 2013 (SCI-Expanded) identifier identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 339 Sayı: 6120
  • Basım Tarihi: 2013
  • Doi Numarası: 10.1126/science.1231382
  • Dergi Adı: SCIENCE
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Sayfa Sayıları: ss.698-699
  • Bursa Uludağ Üniversitesi Adresli: Evet

Özet

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.