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Mutation spectrum data for Saccharomyces cerevisiae psf1-1 pol2-M644G mutants
Michal Dmowski1, Karolina Makiela-Dzbenska1, Malgorzata Jedrychowska1
1Institute of Biochemistry and Biophysics, Polish Academy of Sciences, Pawinskiego 5A, 02-106 Warsaw, Poland.
Data in Brief
|May 23, 2022
Summary
Investigating DNA replication in yeast, this study reveals that impairing the CMG helicase complex increases the role of DNA polymerase delta in leading strand synthesis. This finding offers new insights into DNA repair mechanisms.
Area of Science:
- Molecular Biology
- Genetics
- Biochemistry
Background:
- DNA replication is crucial for cell division, with distinct polymerases handling leading and lagging strands.
- Polymerase epsilon (Pol ε) primarily synthesizes the leading strand, while Polymerase delta (Pol δ) handles the lagging strand in eukaryotes.
- The GINS complex, along with Cdc45 and Mcm2-7, forms the CMG helicase complex, essential for recruiting Pol ε.
Purpose of the Study:
- To analyze the contribution of Pol ε to DNA replication in yeast with a defective GINS complex.
- To investigate how impaired CMG helicase function affects the roles of DNA polymerases.
- To observe changes in mutational spectra resulting from altered DNA replication dynamics.
Main Methods:
- Utilized the pol2-M644G mutant allele of Pol ε to track its activity.
- Employed the psf1-1 mutant allele affecting the GINS complex in *Saccharomyces cerevisiae*.
- Analyzed DNA sequencing data from the URA3 reporter gene in different orientations relative to ARS.
Main Results:
- Observed alterations in mutational spectra within the URA3 reporter gene.
- Data suggest a shift in polymerase activity during replication under impaired CMG helicase function.
- The study supports findings of increased Pol δ involvement in leading strand replication.
Conclusions:
- Impaired CMG helicase complex function influences DNA polymerase recruitment and activity.
- This can lead to an increased contribution of DNA polymerase delta to leading strand synthesis.
- Understanding these dynamics is vital for comprehending genome stability and replication fidelity.

