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Updated: May 10, 2026

In Vitro Chemical Mapping of G-Quadruplex DNA Structures by Bis-3-Chloropiperidines

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Published on: May 12, 2023

Pentose phosphate pathway function affects tolerance to the G-quadruplex binder TMPyP4.

Elizabeth J Andrew¹, Stephanie Merchan, Conor Lawless

¹Institute for Cell and Molecular Biosciences, Newcastle University Medical School, Newcastle Upon Tyne, United Kingdom.

|June 19, 2013

Summary

This summary is machine-generated.

The anti-cancer drug candidate TMPyP4 causes light-dependent oxidative stress in yeast, not G-quadruplex binding. This finding impacts the drug

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Nucleoside Triphosphates - From Synthesis to Biochemical Characterization

Nucleoside Triphosphates - From Synthesis to Biochemical Characterization

Published on: April 3, 2014

Area of Science:

Molecular Biology
Genetics
Biochemistry

Background:

G-quadruplexes are DNA structures found in guanine-rich regions, particularly at telomeres.
Ligands like TMPyP4 stabilize G-quadruplexes and are investigated as anti-cancer agents.
Understanding TMPyP4's in vivo mechanism is crucial for its therapeutic potential.

Purpose of the Study:

To elucidate the in vivo mechanism of action of the G-quadruplex ligand TMPyP4.
To identify cellular pathways involved in TMPyP4 sensitivity using a genome-wide screen in Saccharomyces cerevisiae.

Main Methods:

Conducted a genome-wide screen in budding yeast (Saccharomyces cerevisiae) to identify genes affecting TMPyP4 sensitivity.
Assessed sensitivity to TMPyP4, hydrogen peroxide, RHPS4, and hydroxyurea in gene deletion strains.
Investigated the role of the pentose phosphate pathway (PPP) and oxidative stress response genes (CCS1, YAP1).

Main Results:

Deletion of key pentose phosphate pathway (PPP) genes increased yeast sensitivity to TMPyP4.
Sensitivity to TMPyP4 was also elevated in strains lacking oxidative stress response genes (CCS1, YAP1).
TMPyP4-sensitive strains showed cross-sensitivity to hydrogen peroxide, suggesting a role for oxidative stress.

Conclusions:

TMPyP4 treatment induces a light-dependent oxidative stress response in budding yeast.
Oxidative stress, rather than direct G-quadruplex binding, appears to be the primary mechanism of TMPyP4 cytotoxicity.
Findings have significant implications for the therapeutic application and understanding of TMPyP4's mechanism of action.