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Related Concept Videos

In-vitro Mutagenesis01:16

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.
Gene Conversion02:08

Gene Conversion

Other than maintaining genome stability via DNA repair, homologous recombination plays an important role in diversifying the genome. In fact, the recombination of sequences forms the molecular basis of genomic evolution. Random and non-random permutations of genomic sequences create a library of new amalgamated sequences. These newly formed genomes can determine the fitness and survival of cells. In bacteria, homologous and non-homologous types of recombination lead to the evolution of new...
Mismatch Repair01:20

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...
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Overview
Overview of Transposition and Recombination02:13

Overview of Transposition and Recombination

Transposons make up a significant part of genomes of various organisms. Therefore, it is believed that transposition played a major evolutionary role in speciation by changing genome sizes and modifying gene expression patterns. For example, in bacteria, transposition can lead to conferring antibiotic resistance. Movement of transposable elements within the genetic pool of pathogenic bacteria can aid in transfer of antibiotic-resistant genetic elements. In eukaryotes, transposons can carry out...
In vitro Mutagenesis01:16

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.

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Related Experiment Video

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Optogenetic Random Mutagenesis Using Histone-miniSOG in C. elegans
04:51

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Published on: November 14, 2016

Tagged mutagenesis by efficient Minos-based germ line transposition.

Ton de Wit1, Sylvia Dekker, Alex Maas

  • 1Department of Cell Biology, Erasmus Medical Center, Rotterdam, The Netherlands.

Molecular and Cellular Biology
|November 4, 2009
PubMed
Summary

Researchers developed a new mouse model system using Minos transposon technology for efficient gene mutation generation. This system rapidly identifies genes causing cardiovascular disease and aids in modifier gene screening.

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Area of Science:

  • Genetics and Genomics
  • Developmental Biology
  • Transposon Technology

Background:

  • Germ line gene transposition is crucial for creating mutant libraries in model organisms like flies and worms.
  • Existing methods for generating mouse mutants in vivo are often slow and inefficient.
  • There is a significant need for rapid and effective mouse mutant generation to study developmental defects and human diseases.

Purpose of the Study:

  • To describe an optimized mammalian germ line transposition system for early mouse spermatogenesis.
  • To utilize the Minos transposon for efficient in vivo generation of mouse mutants.
  • To establish a rapid screening system for identifying genes associated with cardiovascular disease phenotypes.

Main Methods:

  • Development and optimization of a Minos transposon-based germ line transposition system in mice.
  • Activation of transposition during early mouse spermatogenesis.
  • Functional screening of resulting mouse mutants for cardiovascular disease phenotypes.

Main Results:

  • The optimized system achieved an average of over 2 new transpositions per transposon-positive progeny.
  • 45% to 100% of progeny carried a gene insertion, demonstrating high efficiency.
  • The system successfully identified mutated genes causing measurable cardiovascular disease phenotypes in a rapid dominant screen.

Conclusions:

  • The optimized Minos transposon system provides a fast and efficient method for generating mouse mutants in vivo.
  • This technology facilitates the modeling of developmental defects and human diseases, particularly cardiovascular conditions.
  • The system is valuable for rapid screening of both disease-causing and modifier genes.