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 Blood, 15 June 2006, Vol. 107, No. 12, pp. 4898-4906.
Prepublished online as a Blood First Edition Paper on February 21, 2006; DOI 10.1182/blood-2005-09-3596.

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NEOPLASIA

Clarifying the role of Stat5 in lymphoid development and Abelson-induced transformation

Andrea Hoelbl, Boris Kovacic, Marc A. Kerenyi, Olivia Simma, Wolfgang Warsch, Yongzhi Cui, Hartmut Beug, Lothar Hennighausen, Richard Moriggl, and Veronika Sexl

From the Institute of Pharmacology and Max F. Perutz Laboratories, Medical University of Vienna (MUW), Austria; Institute of Molecular Pathology (IMP), Vienna, Austria; Laboratory of Genetics and Physiology, National Institutes of Health (NIH), Bethesda, MD; and Ludwig Boltzmann Institute for Cancer Research (LBI-CR), Vienna, Austria.

The Stat5 transcription factors Stat5a and Stat5b have been implicated in lymphoid development and transformation. Most studies have employed Stat5a/b-deficient mice where gene targeting disrupted the first protein-coding exon, resulting in the expression of N-terminally truncated forms of Stat5a/b (Stat5a/b{Delta}N/{Delta}N mice). We have now reanalyzed lymphoid development in Stat5a/bnull/null mice having a complete deletion of the Stat5a/b gene locus. The few surviving Stat5a/bnull/null mice lacked CD8+ T lymphocytes. A massive reduction of CD8+ T cells was also found in Stat5a/bfl/fl lck-cre transgenic animals. While {gamma}{delta} T-cell receptor–positive ({gamma}{delta}TCR+) cells were expressed at normal levels in Stat5a/b{Delta}N/{Delta}N mice, they were completely absent in Stat5a/bnull/null animals. Moreover, B-cell maturation was abrogated at the pre–pro-B-cell stage in Stat5a/bnull/null mice, whereas Stat5a/b{Delta}N/{Delta}N B-lymphoid cells developed to the early pro-B-cell stage. In vitro assays using fetal liver-cell cultures confirmed this observation. Most strikingly, Stat5a/bnull/null cells were resistant to transformation and leukemia development induced by Abelson oncogenes, whereas Stat5a/b{Delta}N/{Delta}N-derived cells readily transformed. These findings show distinct lymphoid defects for Stat5a/b{Delta}N/{Delta}N and Stat5a/bnull/null mice and define a novel functional role for the N-termini of Stat5a/b in B-lymphoid transformation.


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