Related Experiment Video
Updated: Aug 7, 2026
08:28
Single-molecule Manipulation of G-quadruplexes by Magnetic Tweezers
Published on: September 19, 2017
Specific interactions of distamycin with G-quadruplex DNA
Melanie J Cocco1, L A Hanakahi, Michael D Huber
1Department of Molecular Biophysics and Biochemistry, Yale University, New Haven, CT 06520, USA. cocco@csb.yale.edu
Nucleic Acids Research
|May 29, 2003
Summary
Distamycin, a DNA-binding molecule, can inhibit protein interactions with G-quadruplex (G4) DNA. This study reveals distamycin
Area of Science:
- Molecular Biology
- Biochemistry
- Structural Biology
Background:
- Distamycin is known to bind the minor groove of duplex DNA, particularly AT-rich regions.
- This interaction makes it a useful tool for studying protein interactions with double-stranded DNA.
- G-quadruplex (G4) DNA is a stable, four-stranded nucleic acid structure with implications in various biological processes.
Purpose of the Study:
- To investigate the interaction of distamycin with G-quadruplex (G4) DNA.
- To determine if distamycin can inhibit protein interactions with G4 DNA.
- To characterize the binding mode of distamycin to G4 DNA.
Main Methods:
- Nuclear Magnetic Resonance (NMR) spectroscopy was employed to study the binding of distamycin to G4 DNA.
- Structural analysis of the distamycin-G4 DNA complex.
Main Results:
- Distamycin was found to inhibit protein interactions with G4 DNA.
- NMR data confirmed specific binding of distamycin to G4 DNA.
- Distamycin stacks on the terminal G-quartets and interacts with flanking bases within the G4 structure.
Conclusions:
- Distamycin serves as a valuable probe for studying G-quadruplex DNA-protein interactions.
- The findings suggest at least two distinct modes of protein recognition for G4 DNA.
- These modes can be differentiated based on their sensitivity to distamycin inhibition.
Related Concept Videos
02:36DNA Damage can Stall the Cell Cycle
In response to DNA damage, cells can pause the cell cycle to assess and repair the breaks. However, the cell must check the DNA at certain critical stages during the cell cycle. If the cell cycle pauses before DNA replication, the cells will contain twice the amount of DNA. On the other hand, if cells arrest after DNA replication but before mitosis, they will contain four times the normal amount of DNA. With a host of specialized proteins at their disposal,cells must use the right protein at...
02:37Restarting Stalled Replication Forks
DNA replication is initiated at sites containing predefined DNA sequences known as origins of replication. DNA is unwound at these sites by the minichromosome maintenance (MCM) helicase and other factors such as Cdc45 and the associated GINS complex.The unwound single strands are protected by replication protein A (RPA) until DNA polymerase starts synthesizing DNA at the 5’ end of the strand in the same direction as the replication fork. To prevent the replication fork from falling apart, a...
01:03Single-Strand DNA Binding Proteins
For successful DNA replication, the unwinding of double-stranded DNA must be accompanied by stabilization and protection of the separated single strands of the DNA. This crucial task is performed by single-strand DNA-binding (SSB) proteins. They bind to the DNA in a sequence-independent manner, which means that the nitrogenous bases of the DNA need not be present in a specific order for binding of SSB proteins to it. The binding of SSB proteins straightens single-stranded DNA (ssDNA) and makes...
01:10Drugs that Destabilize Microtubules
Microtubules are dynamic structures and can be regulated by microtubule targeting agents (MTAs). Microtubule destabilizing drugs are a class of MTAs that destabilize and prevent microtubules' polymerization. Both natural and synthetic chemicals can be found under this class of drugs. Vincristine and vinblastine, two vinca alkaloids, and colchicine were among the first to be discovered. These drugs can affect cells in various ways, either by inducing a change in cell morphology, preventing...
01:28Inhibitors of Bacterial DNA Synthesis
Bacterial pathogens depend on precise and efficient DNA replication to sustain infection. Two type II topoisomerases—DNA gyrase and topoisomerase IV—are critical to this process, as they resolve DNA supercoiling and unlink chromosomes during replication. Fluoroquinolones, synthetic derivatives of quinolones, exploit this mechanism by stabilizing the transient DNA–enzyme cleavage complex, preventing strand religation, and causing lethal double-strand breaks. These antibiotics are selectively...