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Perinatal lethality and blocked B-cell development in mice lacking the tyrosine kinase Syk

Turner, Martin, Joseph Mee, P., Costello, Patrick S., Williams, Owen, Price, Abigail A., Duddy, Linda P., Furlong, Michael T., Geahlen, Robert L., Tybulewicz, Victor L. J.·1995·Nature
DOI 10.1038/378298a0
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Abstract

The tyrosine kinase Syk (relative molecular mass 72,000), which is widely expressed in haematopoietic cells, becomes associated with and activated by engagement of the B-cell antigen receptor. Furthermore, it has been implicated in signalling through the receptors for interleukin-2 (IL-2), granulocyte colony-stimulating factor (G-CSF) and Fc, the T cell receptor, as well as through receptors for several platelet agonists. A homologous kinase, ZAP-70, is crucial in signalling through the T-cell receptor and in T-cell development. Using homologous recombination in embryonic stem cells, we created mice null for the syk gene which showed petechiae in utero and died shortly after birth. Irradiated mice reconstituted with Syk-deficient fetal liver showed a block in B-cell development at the pro-B to pre-B cell transition, consistent with a key role for Syk in pre-B-cell receptor signalling. Despite the production of small numbers of immature B cells, Syk-deficient radiation chimaeras failed to accumulate mature B cells, indicating a possible role for this protein in the production or maintenance of mature B cells. In addition, whereas the development of alpha beta T cells proceeded normally, Syk-deficient mice showed impaired development of thymocytes using the V gamma 3 variable region gene (V gamma 3+ thymocytes). Finally, we show that Syk is not required for signalling through the IL-2 and G-CSF receptors.

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Metadata

Authors
Turner, M., Joseph Mee, P., Costello, P. S., Williams, O., Price, A. A., Duddy, L. P., Furlong, M. T., Geahlen, R. L., & Tybulewicz, V. L. J.
Venue
Nature
Publisher
Springer Science and Business Media LLC
Published
1995-11
Volume
378
Issue
6554
Pages
298-302
ISSN
  • 0028-0836
  • 1476-4687
DOI
10.1038/378298a0
Cited by
612
References
0
Language
en
Licence
www.springer.com/tdm (tdm)

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