Rapid in vivo analysis of mutant forms of the LAT adaptor using Pax5-Lat double-deficient pro-B cells

Eur J Immunol. 2005 Mar;35(3):977-86. doi: 10.1002/eji.200425836.

Abstract

Following injection into recombinase-activating gene-deficient (Rag1(-/-)) mice, pro-B cells lacking the Pax5 transcription factor (Pax5(-/-)) develop into most major hematopoietic lineages, with the notable exception of B cells. We assessed whether Pax5(-/-) pro-B cells that were also rendered deficient for the linker for activation of T cells (LAT), an adaptor essential for T cell receptor signaling, can be used for the rapid in vivo analysis of mutant forms of LAT. We showed that Pax5(-/-) Lat(-/-) pro-B cell lines can be infected with recombinant retroviruses expressing a LAT cDNA and sorted for the expression of LAT. When injected into Rag1(-/-) mice, they restore normal intrathymic T cell development and give rise to functional peripheral T cells. Considering that the handling of Pax5(-/-) pro-B cell lines is easier than that of bone marrow hematopoietic precursors, we used them for the rapid functional analysis of a novel Lat allelic series. When compared to knock-in and transgenic approaches, a major advantage of our Pax5(-/-) pro-B cell-based experimental approach consists in the production of mice bearing a given mutation within 2-3 months. Therefore, it constitutes a powerful first-line screen for mutations worth fastidious knock-in approaches.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adaptor Proteins, Signal Transducing / deficiency
  • Adaptor Proteins, Signal Transducing / genetics*
  • Adaptor Proteins, Signal Transducing / immunology
  • Animals
  • B-Lymphocytes / immunology*
  • Cell Differentiation / immunology
  • Cells, Cultured
  • DNA-Binding Proteins / deficiency*
  • DNA-Binding Proteins / genetics
  • DNA-Binding Proteins / immunology
  • Flow Cytometry
  • Genetic Techniques*
  • Membrane Proteins / deficiency
  • Membrane Proteins / genetics*
  • Membrane Proteins / immunology
  • Mice
  • Mice, Mutant Strains
  • Mutation
  • PAX5 Transcription Factor
  • Phosphoproteins / deficiency
  • Phosphoproteins / genetics*
  • Phosphoproteins / immunology
  • Stem Cells / cytology
  • Stem Cells / immunology
  • T-Lymphocytes / cytology*
  • T-Lymphocytes / immunology
  • Transcription Factors / deficiency*
  • Transcription Factors / genetics
  • Transcription Factors / immunology

Substances

  • Adaptor Proteins, Signal Transducing
  • DNA-Binding Proteins
  • Lat protein, mouse
  • Membrane Proteins
  • PAX5 Transcription Factor
  • Pax5 protein, mouse
  • Phosphoproteins
  • Slc50a1 protein, mouse
  • Transcription Factors