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Gene expression profile of B cells from Xid mice and Btk knockout mice
Author(s) -
Lindvall Jessica M.,
Blomberg K. Emelie M.,
Berglöf Anna,
Yang Qian,
Smith C. I. Edvard,
Islam Tahmina C.
Publication year - 2004
Publication title -
european journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.272
H-Index - 201
eISSN - 1521-4141
pISSN - 0014-2980
DOI - 10.1002/eji.200324051
Subject(s) - bruton's tyrosine kinase , biology , gene , phenotype , gene knockout , microbiology and biotechnology , mutant , tyrosine kinase , genetics , immunology , signal transduction
Abstract Bruton's tyrosine kinase (Btk) is important for B lymphocyte development. To identify genes that are differentially expressed in primary B cells lacking functional Btk, splenocytes from X‐linked immunodeficiency (Xid), Btk knockout (Btk KO) and immunocompetent CBA mice were used in microarrays containing more than 12,000 genes and expressed‐sequence tags. We found 4515 common transcripts expressed in duplicate experiments in the three strains. Out of these, 38 were differentially expressed genes (21 were up‐regulated >2‐fold and 17 were down‐regulated <–2‐fold) between CBA and Btk defective (Xid or Btk KO) mice. Ten out of these genes were selected and quantitative real‐time PCR was conducted for validation and further investigation. Real‐time experiments correlated nicely with the microarray data. No definitive phenotypic difference has previously been reported between Xid and Btk KO mice. We found 7 genes whose expression differed (>2‐fold) betweenthe two strains. Moreover, when the 38 genes that differed between immunocompetent CBA mice and Btk defective mice were ranked according to fold‐increase, the levels in Btk KO mice were significantly more altered. This suggests that the defect in Btk KO mice is more severe and demonstrates that the mutant Btk protein in Xid mice does not generally function as dominant‐negative form.