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The Hox proteins Ubx and AbdA collaborate with the transcription pausing factor M1 BP to regulate gene transcription
Author(s) -
Zouaz Amel,
Auradkar Ankush,
Delfini Marie Claire,
Macchi Meiggie,
Barthez Marine,
Ela Akoa Serge,
Bastianelli Leila,
Xie Gengqiang,
Deng WuMin,
Levine Stuart S,
Graba Yacine,
Saurin Andrew J
Publication year - 2017
Publication title -
the embo journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 7.484
H-Index - 392
eISSN - 1460-2075
pISSN - 0261-4189
DOI - 10.15252/embj.201695751
Subject(s) - rna polymerase ii , biology , promoter , transcription factor ii d , h3k4me3 , transcription factor ii e , transcription factor , transcription (linguistics) , transcription factor ii f , general transcription factor , ultrabithorax , genetics , sp3 transcription factor , taf2 , chromatin , microbiology and biotechnology , gene , hox gene , gene expression , linguistics , philosophy
In metazoans, the pausing of RNA polymerase II at the promoter (paused Pol II ) has emerged as a widespread and conserved mechanism in the regulation of gene transcription. While critical in recruiting Pol II to the promoter, the role transcription factors play in transitioning paused Pol II into productive Pol II is, however, little known. By studying how Drosophila Hox transcription factors control transcription, we uncovered a molecular mechanism that increases productive transcription. We found that the Hox proteins AbdA and Ubx target gene promoters previously bound by the transcription pausing factor M1 BP , containing paused Pol II and enriched with promoter‐proximal Polycomb Group (PcG) proteins, yet lacking the classical H3K27me3 PcG signature. We found that AbdA binding to M1 BP ‐regulated genes results in reduction in PcG binding, the release of paused Pol II , increases in promoter H3K4me3 histone marks and increased gene transcription. Linking transcription factors, PcG proteins and paused Pol II states, these data identify a two‐step mechanism of Hox‐driven transcription, with M1 BP binding leading to Pol II recruitment followed by AbdA targeting, which results in a change in the chromatin landscape and enhanced transcription.