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PHF3 regulates neuronal gene expression through the Pol II CTD reader domain SPOC
Lisa-Marie Appel1, Vedran Franke2, Melania Bruno1
1Department of Biochemistry and Cell Biology, Max Perutz Labs, University of Vienna, Vienna Biocenter (VBC), Vienna, Austria.
Nature Communications
|October 20, 2021
Summary
PHD-finger protein 3 (PHF3) regulates transcription and mRNA stability by binding the RNA polymerase II CTD. PHF3 impacts neuronal gene expression and differentiation by linking transcription to mRNA decay.
Area of Science:
- Molecular Biology
- Gene Regulation
- Biochemistry
Background:
- The C-terminal domain (CTD) of RNA polymerase II (Pol II) is crucial for transcription and RNA processing.
- PHD-finger protein 3 (PHF3) is identified as a novel regulator in these processes.
Purpose of the Study:
- To investigate the role of PHF3 in transcription and mRNA stability.
- To characterize the interaction between PHF3 and the Pol II CTD.
Main Methods:
- SPOC domain characterization as a CTD reader.
- Analysis of PHF3's effect on Pol II dynamics using knock-out and deletion models.
- Assessment of gene expression and cellular differentiation in PHF3-deficient cells.
Main Results:
- PHF3 docks onto the Pol II CTD via its SPOC domain, recognizing phosphorylated Serine-2 marks.
- PHF3 promotes liquid-liquid phase separation of phosphorylated Pol II and tracks Pol II along genes.
- PHF3 deficiency leads to increased Pol II stalling, reduced elongation, enhanced mRNA stability, and impaired neuronal gene expression and differentiation.
Conclusions:
- PHF3 is a key regulator of neuronal gene expression, bridging transcription and mRNA decay.
- The SPOC domain of PHF3 acts as a CTD reader, influencing Pol II function.
- PHF3 plays a significant role in neuronal differentiation by modulating gene expression patterns.
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