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Updated: May 10, 2026
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Metal-Limited Growth of Neisseria gonorrhoeae for Characterization of Metal-Responsive Genes and Metal Acquisition from Host Ligands
Published on: March 4, 2020
RNA polymerase I stability couples cellular growth to metal availability
Yueh-Jung Lee1, Chrissie Young Lee, Agnieszka Grzechnik
1Department of Chemistry and Biochemistry and the Molecular Biology Institute, University of California, Los Angeles, CA 90095-1569, USA.
Molecular Cell
|June 11, 2013
Summary
Cellular zinc levels control RNA polymerase I stability. In zinc deficiency, RNA polymerase I is degraded, allowing essential gene expression and survival during starvation.
Area of Science:
- Molecular Biology
- Cell Biology
- Biochemistry
Background:
- Zinc is vital for eukaryotic RNA polymerases.
- Regulation of RNA polymerase activity by zinc levels is poorly understood.
Purpose of the Study:
- To investigate how cellular zinc availability affects RNA polymerase activity and stability.
- To elucidate the regulatory mechanisms coordinating transcriptional activity with zinc levels.
Main Methods:
- In vivo studies of RNA polymerase I (RNAPI) stability under varying zinc conditions.
- Analysis of proteolysis, vacuolar degradation pathways, and protein deubiquitination.
- Investigated the roles of Xpo1p, Ubp2p, and Ubp4p in RNAPI regulation.
Main Results:
- RNAPI stability is directly linked to cellular zinc availability.
- Zinc deficiency triggers specific RNAPI degradation via vacuolar proteolysis.
- This degradation pathway involves Xpo1p export and Ubp2p/Ubp4p deubiquitination of Rpa190p.
- RNA polymerase II (RNAPII) activity remains unaffected, preserving essential gene expression.
- RNAPI export to the vacuole is crucial for survival during zinc starvation.
Conclusions:
- A hierarchy of transcriptional activity is established during zinc starvation.
- Degradation of RNAPI couples cellular growth and proliferation to zinc availability.
- RNAPI degradation may serve as a zinc reservoir mechanism.
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