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Mismatch Repair

Mismatch Repair

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...

In vitro Mutagenesis

In vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

Spontaneous and Induced Mutations

Spontaneous and Induced Mutations

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).

In-vitro Mutagenesis

In-vitro Mutagenesis

To learn more about the function of a gene, researchers can observe what happens when the gene is inactivated or “knocked out,” by creating genetically engineered knockout animals. Knockout mice have been particularly useful as models for human diseases such as cancer, Parkinson’s disease, and diabetes.

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

Adaptive Mechanisms in Cancer Cells

Adaptive Mechanisms in Cancer Cells

Cancer cells accumulate genetic changes at an abnormally rapid rate due to the defects in the DNA repair mechanisms. From an evolutionary perspective, such genetic instability is advantageous for cancer development. Mutant cell lines accumulate a series of beneficial mutations that contribute to their progression into cancer.
Some of the advantages that cancer cells have on normal cells include - enhanced ability to divide without terminally differentiating, induce new blood vessel formation,...

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Related Experiment Video

Updated: Jul 2, 2026

Following the Dynamics of Structural Variants in Experimentally Evolved Populations

Following the Dynamics of Structural Variants in Experimentally Evolved Populations

Published on: February 3, 2023

A new experimental system for study on adaptive mutations.

Z Lü¹, A Wang

¹Institute of Microbiology, Chinese Academy of Sciences, 100080, Beijing, China.

Science in China. Series C, Life Sciences

|September 3, 2008

Summary

This summary is machine-generated.

Adaptive mutations can occur in regulatory genes, not just structural genes. This study introduces a new system for investigating adaptive mutations in Salmonella typhimurium.

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Procedure for Adaptive Laboratory Evolution of Microorganisms Using a Chemostat

Procedure for Adaptive Laboratory Evolution of Microorganisms Using a Chemostat

Published on: September 20, 2016

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Last Updated: Jul 2, 2026

Following the Dynamics of Structural Variants in Experimentally Evolved Populations

Following the Dynamics of Structural Variants in Experimentally Evolved Populations

Published on: February 3, 2023

Procedure for Adaptive Laboratory Evolution of Microorganisms Using a Chemostat

Procedure for Adaptive Laboratory Evolution of Microorganisms Using a Chemostat

Published on: September 20, 2016

Area of Science:

Microbiology
Genetics
Molecular Biology

Background:

A super-repressed purR mutant (purR(S)) in Salmonella typhimurium exhibits slow growth on specific media.
This mutant struggles to form colonies when lactose is the sole carbon source, requiring adenine supplementation.

Purpose of the Study:

To investigate the phenomenon of late-arising mutations in purR(S) mutants under non-lethal selection.
To determine if these late-arising mutations are adaptive and to identify the target genes involved.
To extend the understanding of adaptive mutation targets beyond structural genes to regulatory genes.

Main Methods:

Utilizing NCE medium with adenine and lactose for selection.
Employing prolonged non-lethal selection on purR(S) mutants.
Conducting reconstruction experiments with revertants.
Performing statistical analysis (Poisson distribution) on mutant distribution.
Utilizing co-transductional analysis to identify mutation sites.

Main Results:

A phenomenon of late-arising mutations was observed in purR(S) mutants.
Reconstruction experiments confirmed these are not slow-growing mutants.
Statistical analysis indicated mutations occurred post-plating (Poisson distribution).
Co-transductional analysis suggested mutations occurred in the purR gene or the PUR box cis-element of the purD gene.
This study demonstrates adaptive mutations can target trans-regulatory genes.

Conclusions:

The observed late-arising mutations are adaptive, distinct from random mutations.
This research provides the first evidence of adaptive mutations occurring in a trans-regulatory gene (repressor protein).
A novel system for studying adaptive mutations has been established, broadening their known targets.