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Related Concept Videos

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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Nucleotide Excision Repair01:38

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DNA Distortion and Damage
Cells are regularly exposed to mutagens—factors in the environment that can damage DNA and generate mutations. UV radiation is one of the most common mutagens and is estimated to introduce a significant number of changes in DNA. These include bends or kinks in the structure, which can block DNA replication or transcription. If these errors are not fixed, the damage can cause mutations, which in turn can result in cancer or disease depending on which sequences are...
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Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
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Published on: November 1, 2011

Mutations affecting a putative MutLalpha endonuclease motif impact multiple mismatch repair functions.

Naz Erdeniz1, Megan Nguyen, Suzanne M Deschênes

  • 1Department of Molecular and Medical Genetics, Oregon Health & Science University L103, 3181 SW Sam Jackson Park Road, Portland, OR 97239-3098, USA.

DNA Repair
|June 15, 2007
PubMed
Summary

Mutations in DNA mismatch repair (MMR) affect DNA repair, recombination, and cellular responses to methylating agents. The endonuclease activity of MutLalpha is crucial for these DNA repair and damage response functions.

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Assessing Somatic Hypermutation in Ramos B Cells after Overexpression or Knockdown of Specific Genes
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Published on: August 21, 2021

Area of Science:

  • Molecular Biology
  • Genetics
  • Biochemistry

Background:

  • DNA mismatch repair (MMR) corrects errors during DNA replication.
  • Mutations in MMR genes increase mutation rates and affect recombination.
  • Human MutLalpha, a component of MMR, possesses latent endonuclease activity.

Purpose of the Study:

  • To investigate the in vivo role of the endonuclease activity of MutLalpha.
  • To determine if mutations affecting the endonuclease motif impact MMR functions beyond mutation avoidance.

Main Methods:

  • In vivo studies using yeast and mammalian cells.
  • Analysis of mutations impacting the conserved endonuclease motif in PMS2.
  • Assessment of MMR-dependent suppression of homeologous recombination.
  • Evaluation of cellular responses to S(n)1-type methylating agents.

Main Results:

  • Mutations in the endonuclease motif of PMS2 significantly affect MMR-dependent suppression of homeologous recombination in yeast.
  • These mutations also impact cellular responses to S(n)1-type methylating agents in both yeast and mammalian cells.
  • Loss-of-function alleles for mutation avoidance also impaired recombination suppression and damage response.

Conclusions:

  • The endonuclease activity of MutLalpha is essential for multiple MMR functions, including mutation avoidance, suppression of homeologous recombination, and DNA damage response.
  • These findings highlight the multifaceted role of MutLalpha's endonuclease activity in maintaining genome stability.