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TitleArchitecture of Pol II(G) and molecular mechanism of transcription regulation by Gdown1.
Journal, issue, pagesNat Struct Mol Biol, Vol. 25, Issue 9, Page 859-867, Year 2018
Publish dateSep 6, 2018
AuthorsMiki Jishage / Xiaodi Yu / Yi Shi / Sai J Ganesan / Wei-Yi Chen / Andrej Sali / Brian T Chait / Francisco J Asturias / Robert G Roeder /
PubMed AbstractTight binding of Gdown1 represses RNA polymerase II (Pol II) function in a manner that is reversed by Mediator, but the structural basis of these processes is unclear. Although Gdown1 is ...Tight binding of Gdown1 represses RNA polymerase II (Pol II) function in a manner that is reversed by Mediator, but the structural basis of these processes is unclear. Although Gdown1 is intrinsically disordered, its Pol II interacting domains were localized and shown to occlude transcription factor IIF (TFIIF) and transcription factor IIB (TFIIB) binding by perfect positioning on their Pol II interaction sites. Robust binding of Gdown1 to Pol II is established by cooperative interactions of a strong Pol II binding region and two weaker binding modulatory regions, thus providing a mechanism both for tight Pol II binding and transcription inhibition and for its reversal. In support of a physiological function for Gdown1 in transcription repression, Gdown1 co-localizes with Pol II in transcriptionally silent nuclei of early Drosophila embryos but re-localizes to the cytoplasm during zygotic genome activation. Our study reveals a self-inactivation through Gdown1 binding as a unique mode of repression in Pol II function.
External linksNat Struct Mol Biol / PubMed:30190596 / PubMed Central
MethodsEM (single particle)
Resolution3.9 - 4.3 Å
Structure data

7997

6drd

EMDB-7997, PDB-6drd:
RNA Pol II(G)
Method: EM (single particle) / Resolution: 3.9 Å

EMDB-7998:
RNA Pol II(G) focus refinement
Method: EM (single particle) / Resolution: 4.3 Å

Chemicals

ChemComp-ZN:
Unknown entry

Source
  • homo sapiens (human)
  • Human (human)
KeywordsTRANSFERASE / RNA Pol II(G) / Gdown1 / transcription repression / molecular mechanism

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