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Published on: May 15, 2018
High-throughput mutagenesis reveals unique structural features of human ADAR1
SeHee Park1, Erin E Doherty1, Yixuan Xie1
1Department of Chemistry, University of California, Davis, Davis, CA, USA.
Abstract:
Adenosine Deaminases that act on RNA (ADARs) are enzymes that catalyze adenosine to inosine conversion in dsRNA, a common form of RNA editing. Mutations in the human ADAR1 gene are known to cause disease and recent studies have identified ADAR1 as a potential therapeutic target for a subset of cancers. However, efforts to define the mechanistic effects for disease associated ADAR1 mutations and the rational design of ADAR1 inhibitors are limited by a lack of structural information. Here, we describe the combination of high throughput mutagenesis screening studies, biochemical characterization and Rosetta-based structure modeling to identify unique features of ADAR1. Importantly, these studies reveal a previously unknown zinc-binding site on the surface of the ADAR1 deaminase domain which is important for ADAR1 editing activity. Furthermore, we present structural models that explain known properties of this enzyme and make predictions about the role of specific residues in a surface loop unique to ADAR1.
Insights
Researchers uncovered a new zinc-binding site on Adenosine Deaminases that act on RNA 1 (ADAR1), crucial for its RNA editing activity. This discovery aids in understanding disease-related mutations and designing cancer therapies targeting ADAR1.
Area of Science:
- Molecular Biology
- Structural Biology
- Biochemistry
Background:
- Adenosine Deaminases that act on RNA (ADARs) are key enzymes in RNA editing, converting adenosine to inosine in double-stranded RNA (dsRNA).
- The human ADAR1 gene is implicated in various diseases, and ADAR1 is emerging as a therapeutic target for certain cancers.
- A lack of structural information has hindered understanding of ADAR1's disease mechanisms and the development of inhibitors.
Purpose of the Study:
- To elucidate unique structural features of ADAR1 using integrated computational and experimental approaches.
- To identify novel structural elements critical for ADAR1's enzymatic activity.
- To provide a structural basis for understanding ADAR1-associated diseases and guide inhibitor design.
Main Methods:
- High-throughput mutagenesis screening of ADAR1.
- Biochemical characterization of ADAR1 variants.
- Rosetta-based computational structure modeling.
Main Results:
- Identification of a previously unrecognized zinc-binding site on the ADAR1 deaminase domain.
- Demonstration that this zinc-binding site is essential for ADAR1's RNA editing function.
- Development of structural models explaining known ADAR1 properties and predicting residue functions.
Conclusions:
- The newly discovered zinc-binding site is a critical determinant of ADAR1 enzymatic activity.
- Structural insights gained can inform the development of targeted therapies for ADAR1-related diseases and cancers.
- Further investigation into ADAR1's unique surface loop may reveal additional functional mechanisms.
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