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Related Experiment Video

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Measurements of Physiological Stress Responses in C. Elegans

Measurements of Physiological Stress Responses in C. Elegans

Published on: May 21, 2020

The CCAAT-binding complex coordinates the oxidative stress response in eukaryotes.

Marcel Thön¹, Qusai Al Abdallah, Peter Hortschansky

¹Department of Molecular and Applied Microbiology, Leibniz Institute for Natural Product Research and Infection Biology (HKI), Beutenbergstrasse 11a, D-07745 Jena, Germany.

Nucleic Acids Research

|December 8, 2009

Summary

This summary is machine-generated.

The Aspergillus nidulans CCAAT-binding factor (AnCF) redox sensing mechanism involves oxidative modification of HapC, impacting its assembly and DNA binding. This regulation coordinates cellular antioxidant defenses.

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Area of Science:

Molecular Biology
Cellular Biology
Biochemistry

Background:

The CCAAT-binding complex is crucial and conserved across eukaryotes.
In Aspergillus nidulans, this complex (AnCF) comprises HapB, HapC, and HapE subunits, all essential for DNA binding.

Purpose of the Study:

To investigate how the AnCF complex senses and responds to the cell's redox status.
To elucidate the role of HapC modifications in AnCF function and cellular oxidative stress response.

Main Methods:

Utilized mutational analyses to identify key cysteine residues in HapC.
Performed in vitro interaction studies to assess subcomplex formation and DNA binding affinity.
Investigated the effect of hapC gene deletion on oxidative stress response.

Main Results:

Identified oxidative modification of thiol groups in HapC's histone fold motif as the redox sensing mechanism.
Demonstrated that two specific cysteine residues in HapC are critical for AnCF assembly and DNA binding.
Showed that oxidized HapC is sequestered in the cytoplasm but can be reactivated by the thioredoxin system.
Observed an impaired oxidative stress response in cells lacking the hapC gene.

Conclusions:

AnCF is regulated post-transcriptionally by cellular redox status, fine-tuning antioxidant defenses.
This mechanism coordinates the activation/deactivation of genes like NapA and enzymes such as catalase and thioredoxin.
The redox regulation of AnCF likely represents a conserved mechanism in eukaryotic CCAAT-binding complexes.