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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.

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.

Mutagenicity and Carcinogenicity

Mutagenicity and Carcinogenicity

Mutagenicity and carcinogenicity refer to the ability of drugs to cause genetic defects and induce cancer, respectively. The International Agency for Research on Cancer (IARC) classifies agents into four groups based on their carcinogenic potential. Group 1 agents are known human carcinogens; group 2A agents are probably carcinogenic to humans; group 3 agents lack data to support their role in carcinogenesis; and group 4 includes agents for which data support that they are not likely to be...

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...

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).

Viral Mutations

Viral Mutations

A mutation is a change in the sequence of bases of DNA or RNA in a genome. Some mutations occur during replication of the genome due to errors made by the polymerase enzymes that replicate DNA or RNA. Unlike DNA polymerase, RNA polymerase is prone to errors because it is not capable of “proofreading” its work. Viruses with RNA-based genomes, like HIV, therefore accrue mutations faster than viruses with DNA-based genomes. Because mutation and recombination provide the raw material for adaptive...

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Related Experiment Video

Updated: Jun 3, 2026

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Published on: February 24, 2014

HSV Mutagenesis.

¹The Windeyer Institute, London, UK.

Methods in Molecular Medicine

|March 5, 2011

Summary

Understanding herpes virus requires dissecting its complex genome. This involves linking herpes-encoded proteins to their functions and identifying regulatory DNA regions for better control of gene expression.

Area of Science:

Virology
Molecular Biology
Genomics

Background:

Herpes viruses possess large, intricate genomes with numerous interactions between viral components and host cells.
These interactions are crucial from viral entry through the decision between latency and lytic replication.

Purpose of the Study:

To explore the functions of herpes-encoded proteins.
To identify mechanisms controlling herpes gene expression during viral replication and latency.
To link protein-coding regions with specific functions and control DNA regions.

Main Methods:

Fine dissection of the herpes genome.
Analysis of viral protein functions.
Identification of regulatory DNA elements.

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Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Published on: January 26, 2017

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Related Experiment Videos

Last Updated: Jun 3, 2026

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Identifying DNA Mutations in Purified Hematopoietic Stem/Progenitor Cells

Published on: February 24, 2014

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Targeted in Situ Mutagenesis of Histone Genes in Budding Yeast

Published on: January 26, 2017

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Dissecting Host-virus Interaction in Lytic Replication of a Model Herpesvirus

Published on: October 7, 2011

Main Results:

Detailed mapping of herpes-encoded proteins to their functions.
Identification of key DNA regions controlling herpes gene expression.
Understanding of temporal gene expression regulation during the viral life cycle.

Conclusions:

A comprehensive understanding of herpes virus requires detailed genomic dissection.
Linking viral proteins to functions and regulatory DNA is essential for controlling gene expression and viral replication.