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Related Concept Videos

Mutations in Microorganisms01:18

Mutations in Microorganisms

37
Mutations are heritable changes in an organism’s genome involving alterations in the base sequence of DNA or RNA. These changes can influence cellular processes and phenotypic traits, potentially transforming the unaltered wild type into a mutant form. Such changes, termed forward mutations, are pivotal in shaping the genetic diversity of organisms.RNA viruses exhibit the highest mutation rates due to the absence of robust proofreading mechanisms during genome replication. In contrast,...
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Spontaneous and Induced Mutations01:30

Spontaneous and Induced Mutations

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Spontaneous mutations arise infrequently during DNA replication due to errors in the process. A key factor behind these errors is tautomeric shifts in nitrogenous bases, where bases transition from keto to enol forms or amino to imino forms. This shift can alter base-pairing rules, leading to mutations. Additionally, reactive oxygen species (ROS) arising from aerobic metabolism can damage DNA, resulting in depurination (loss of a purine base) or depyrimidination (loss of a pyrimidine base).
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Mismatch Repair01:20

Mismatch Repair

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Organisms are capable of detecting and fixing nucleotide mismatches that occur during DNA replication. This sophisticated process requires identifying the new strand and replacing the erroneous bases with correct nucleotides. Mismatch repair is coordinated by many proteins in both prokaryotes and eukaryotes.
The Mutator Protein Family Plays a Key Role in DNA Mismatch Repair
The human genome has more than 3 billion base pairs of DNA per cell. Prior to cell division, that vast amount of genetic...
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Mutations01:39

Mutations

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Overview
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Genome Copying Errors02:46

Genome Copying Errors

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DNA replication is a well-evolved process that copies millions of base pairs with high fidelity during each cell division. Occasionally a wrong base or a long stretch of wrong bases may get added to the daughter strands. If the errors are left unchecked, cells might accumulate several mutations that might endanger their  survival. Therefore, the copying errors are checked and repaired at three levels.
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Related Experiment Video

Updated: Aug 5, 2025

Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis
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Studying Ribonucleotide Incorporation: Strand-specific Detection of Ribonucleotides in the Yeast Genome and Measuring Ribonucleotide-induced Mutagenesis

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Spontaneous Mutation Rates and Spectra of Respiratory-Deficient Yeast.

Xinyu Tu1, Fan Wang1, Gianni Liti2

  • 1State Key Laboratory of Oncology in South China, Collaborative Innovation Center for Cancer Medicine, Guangdong Key Laboratory of Nasopharyngeal Carcinoma Diagnosis and Therapy, Sun Yat-sen University Cancer Center, Guangzhou 510060, China.

Biomolecules
|March 29, 2023
PubMed
Summary

Mitochondrial dysfunction in yeast causes genome instability, increasing single nucleotide variants and insertions/deletions. Suppressor mutations restore fitness and stability, revealing insights into respiratory deficiency effects.

Keywords:
ATP3MRPL25genome instabilitymtDNA lossmutation raterespiratory deficiency

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Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae
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Combining Magnetic Sorting of Mother Cells and Fluctuation Tests to Analyze Genome Instability During Mitotic Cell Aging in Saccharomyces cerevisiae
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Area of Science:

  • * Molecular and Cellular Biology
  • * Genetics and Genomics
  • * Yeast Model Systems

Background:

  • * The petite phenotype in *Saccharomyces cerevisiae* is linked to respiratory chain defects and mitochondrial genome (mtDNA) loss.
  • * Previous work identified *MRPL25* deletion as a cause of mtDNA loss and the petite phenotype, which can be rescued by *ATP3* mutations.
  • * The *mrpl25Δ* strain exhibited an elevated single nucleotide variant (SNV) rate, indicating genome instability during mtDNA loss.

Purpose of the Study:

  • * To investigate the genome-wide mutation landscape and mutational signatures associated with mitochondrial dysfunction in yeast.
  • * To compare mutation spectra between different types of petite yeast strains and their wild-type counterparts.
  • * To assess the impact of suppressor mutations on genome stability in petite yeast models.

Main Methods:

  • * Whole-genome sequencing of *Saccharomyces cerevisiae* strains with varying *MRPL25* and *ATP3* genotypes.
  • * Analysis of mutation spectra, including single nucleotide variants (SNVs) and insertions/deletions (INDELs).
  • * Comparative analysis of mutation rates and signatures between petite (*mrpl25Δ*, rho0) and wild-type strains.

Main Results:

  • * The *mrpl25Δ* strain showed increased rates of both SNVs and INDELs, confirming genome instability.
  • * Distinct INDEL rates and transition/transversion ratios were observed between *mrpl25Δ* and rho0 petite strains, suggesting different mutational signatures.
  • * Acquisition of *ATP3* suppressor mutations abolished petite-related mutagenesis, restoring both fitness and genome stability.

Conclusions:

  • * Respiratory deficiency in yeast leads to significant genome instability, characterized by elevated SNV and INDEL rates.
  • * Different mechanisms of mitochondrial dysfunction result in distinct mutational signatures.
  • * Suppressor mutations provide a mechanism to restore cellular fitness and genomic integrity in respiratory-deficient yeast.