Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Mutational activity in cell line WEHI-231.

Clifford L Wang1, Matthias Wabl

  • 1Department of Microbiology and Immunology, University of California, San Francisco, CA 94143-0414, USA. mutator@itsa.ucsf.edu

Immunogenetics
|December 18, 2004
PubMed
Summary

The WEHI-231 cell line shows low mutation rates despite normal activation-induced cytidine deaminase (AID) expression. This study reveals significantly reduced C to G and C to T mutational activity, suggesting a defect in DNA repair pathways.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Neoantigen-targeted CD8<sup>+</sup> T cell responses with PD-1 blockade therapy.

Nature·2023
Same author

Non-viral precision T cell receptor replacement for personalized cell therapy.

Nature·2022
Same author

Complete motif analysis of sequence requirements for translation initiation at non-AUG start codons.

Nucleic acids research·2017
Same author

Infectivity and insertional mutagenesis of endogenous retrovirus in autoimmune NZB and B/W mice.

The Journal of general virology·2015
Same author

APOBEC3 enzymes restrict marginal zone B cells.

European journal of immunology·2014
Same author

Evaluation of sgRNA target sites for CRISPR-mediated repression of TP53.

PloS one·2014

Area of Science:

  • Immunology
  • Molecular Biology
  • Genetics

Background:

  • The WEHI-231 cell line expresses activation-induced cytidine deaminase (AID), crucial for B cell hypermutation and immunoglobulin class switch recombination.
  • Despite normal AID expression, WEHI-231 exhibits a low mutation frequency at its endogenous immunoglobulin locus.

Purpose of the Study:

  • To investigate the mutational activity of the WEHI-231 cell line using distinct indicator constructs.
  • To quantify specific mutational activities mediated by AID and identify potential deficiencies in DNA repair.

Main Methods:

  • Utilized three indicator constructs to measure different types of mutations: C to G/C to A transversions, C to G transversions, and C to U deamination (leading to C to T transitions).
  • Compared mutational frequencies in WEHI-231 against a known hypermutating cell line (18-81).

Related Experiment Videos

Main Results:

  • WEHI-231 displayed a 32- to 37-fold reduction in C to G activity compared to the 18-81 cell line.
  • C to T activity was also significantly reduced, approximately 12-fold lower than in the hypermutating control.
  • The data indicates a specific deficiency in pathways responsible for repairing C to U lesions.

Conclusions:

  • The WEHI-231 cell line possesses a defect that impairs the faithful repair of C to U mutations, leading to reduced overall mutational activity.
  • This deficiency likely explains the low mutation frequency observed at the endogenous immunoglobulin locus in this cell line.
  • Further research is needed to identify the specific repair pathway defect in WEHI-231.