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Related Concept Videos

Mutations in Microorganisms01:18

Mutations in Microorganisms

1.2K
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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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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Mismatch Repair01:36

Mismatch Repair

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Overview
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Genome Copying Errors02:46

Genome Copying Errors

4.2K
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.
4.2K
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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Mutations01:39

Mutations

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Related Experiment Video

Updated: Apr 27, 2026

Generation of Genomic Deletions in Mammalian Cell Lines via CRISPR/Cas9
09:40

Generation of Genomic Deletions in Mammalian Cell Lines via CRISPR/Cas9

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Gene deletion speeds mutation rate

    Cancer Discovery
    |July 9, 2014
    PubMed
    Summary

    Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) proteins normally defend against viruses by editing viral genomes. A specific deletion causes numerous human genome mutations, increasing cancer risk.

    Area of Science:

    • Genetics
    • Virology
    • Oncology

    Background:

    • The Apolipoprotein B mRNA editing enzyme, catalytic polypeptide-like (APOBEC) family comprises crucial antiviral factors that function by introducing mutations into viral DNA.
    • APOBEC proteins play a significant role in innate immunity by targeting and modifying viral genomes.

    Discussion:

    • A specific deletion within the APOBEC gene cluster leads to a loss of function for a key APOBEC protein.
    • This deficiency results in a substantial increase in the mutation rate across the human genome.
    • Elevated mutation rates are a known hallmark of cancer development and progression.

    Key Insights:

    • Loss of a specific APOBEC protein through deletion dramatically elevates human genome mutation frequency.
    • This genomic instability is strongly associated with an increased risk of developing various cancers.

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    Generation of Genomic Deletions in Mammalian Cell Lines via CRISPR/Cas9
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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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  • Understanding APOBEC function is critical for both antiviral defense and cancer prevention strategies.
  • Outlook:

    • Further research into APOBEC-mediated mutagenesis can reveal novel therapeutic targets for cancer treatment.
    • Investigating the precise mechanisms linking APOBEC deficiency to oncogenesis may lead to improved cancer diagnostics.
    • Developing strategies to restore or mimic APOBEC function could offer new avenues for cancer chemoprevention.