Mice homozygous for the ablm1 mutation show poor viability and depletion of selected B and T cell populations

Cell. 1991 Jun 28;65(7):1165-75. doi: 10.1016/0092-8674(91)90012-n.


The c-abl gene, originally identified as the cellular homolog of the transforming gene of the Abelson murine leukemia virus, encodes a protein-tyrosine kinase of unknown function that is expressed in all mammalian tissues. We have previously described the introduction of a mutation in the c-abl gene into the mouse germline via targeted gene disruption of embryonic stem cells. We now show that mice homozygous for this mutation are severely affected, displaying increased perinatal mortality, runtedness, and abnormal spleen, head, and eye development. We have examined components of the immune system and have found major reductions in B cell progenitors in the adult bone marrow, with less dramatic reductions in developing T cell compartments.

Publication types

  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • Antigens, Differentiation, B-Lymphocyte / analysis
  • Antigens, Differentiation, T-Lymphocyte / analysis
  • B-Lymphocyte Subsets / cytology
  • Bone Marrow Cells
  • Bone Marrow Transplantation
  • Eye Abnormalities / genetics
  • Flow Cytometry
  • Hematopoiesis*
  • Homozygote
  • Lymphocytes / cytology*
  • Mice
  • Mice, Mutant Strains
  • Oligonucleotides / chemistry
  • Phenotype
  • Phosphorylation
  • Polymerase Chain Reaction
  • Protein-Tyrosine Kinases / metabolism
  • Proto-Oncogene Proteins c-abl / genetics*
  • Spleen / cytology
  • Spleen / pathology
  • T-Lymphocyte Subsets / cytology


  • Antigens, Differentiation, B-Lymphocyte
  • Antigens, Differentiation, T-Lymphocyte
  • Oligonucleotides
  • Protein-Tyrosine Kinases
  • Proto-Oncogene Proteins c-abl