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Mouse strains with point mutations in TAP1 and TAP2.

Angelo Theodoratos1, Belinda Whittle, Anselm Enders

  • 1Biochemistry and Molecular Biology, Research School of Biology, The Australian National University, Canberra, Australia.

Immunology and Cell Biology
|September 2, 2009
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Summary

Two new mouse strains, Jasmine and Rose, with mutations in transporter associated with antigen processing (TAP)1 and TAP2 genes, were developed. These models exhibit reduced immune cell surface markers and offer insights into Bare Lymphocyte syndrome type 1.

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Area of Science:

  • Immunology
  • Genetics
  • Molecular Biology

Background:

  • The transporter associated with antigen processing (TAP) is crucial for presenting antigens to T cells via MHC class I molecules.
  • Defects in TAP lead to immune deficiencies, including Bare Lymphocyte syndrome type 1.
  • Ethyl nitroso urea (ENU) screens are effective for identifying mutations affecting the immune system.

Purpose of the Study:

  • To report the generation and characterization of two novel mouse strains with specific mutations in TAP1 and TAP2.
  • To investigate the functional consequences of these mutations on immune cell surface expression and T cell populations.
  • To establish new animal models for studying human immunodeficiency disorders related to antigen presentation.

Main Methods:

  • Generation of mutant mouse strains (Jasmine and Rose) using ENU mutagenesis.
  • Analysis of major histocompatibility complex (MHC)-I cell-surface expression.
  • Quantification of CD8(+) T cell populations.
  • Genetic sequencing to identify point mutations in TAP1 and TAP2 genes.
  • Assessment of TAP1 and TAP2 protein levels.

Main Results:

  • The Rose strain exhibits a point mutation in TAP1 (Asn643Val), and the Jasmine strain has a mutation in TAP2 (Thr293Pro).
  • Both strains show significantly reduced MHC-I cell-surface expression and diminished CD8(+) T cell numbers.
  • Jasmine mice display severely reduced TAP2 protein levels, with a secondary decrease in TAP1 protein, suggesting a role for TAP2 in TAP1 stabilization.
  • Jasmine is the first available mouse model with a defective TAP2 gene.

Conclusions:

  • The developed Jasmine and Rose mouse strains are valuable models for studying TAP function and associated immune disorders.
  • The findings reveal a novel role for mouse TAP2 in stabilizing TAP1 protein expression.
  • These models advance research into Bare Lymphocyte syndrome type 1 and identify critical residues for TAP function.