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Blood, 15 February 2001, Vol. 97, No. 4, pp. 911-914
HEMATOPOIESIS
Requirement of Shp-2 tyrosine phosphatase in lymphoid and
hematopoietic cell development
Cheng-Kui Qu,
Suzanne Nguyen,
Jianzhu Chen, and
Gen-Sheng Feng
From the Burnham Institute, La Jolla, CA; Department of
Biochemistry and Molecular Biology, Walther Oncology Center, Indiana
University School of Medicine, Indianapolis, IN; and Center for Cancer
Research and Department of Biology, Massachusetts Institute of
Technology, Cambridge, MA.
Shp-1 and Shp-2 are cytoplasmic phosphotyrosine
phosphatases with similar structures. Mice deficient in Shp-2 die at
midgestation with defects in mesodermal patterning, and a hypomorphic
mutation at the Shp-1 locus results in the moth-eaten
viable (mev) phenotype. Previously, a critical role of
Shp-2 in mediating erythroid/myeloid cell development was demonstrated.
By using the RAG-2-deficient blastocyst complementation, the role of
Shp-2 in lymphopoiesis has been determined. Chimeric mice generated by
injecting Shp-2 / embryonic stem cells into
Rag-2-deficient blastocysts had no detectable mature T and B cells,
serum immunoglobulin M, or even Thy-1+ and
B220+ precursor lymphocytes. Collectively, these results
suggest a positive role of Shp-2 in the development of all blood cell
lineages, in contrast to the negative effect of Shp-1 in this process.
To determine whether Shp-1 and Shp-2 interact in hematopoiesis,
Shp-2/:mev/mev double-mutant
embryos were generated and the hematopoietic cell development in the
yolk sacs was examined. More hematopoietic stem/progenitor cells were
detected in Shp-2/:mev/mev
embryos than in Shp-2/ littermates. The partial rescue
by Shp-1 deficiency of the defective hematopoiesis caused by the Shp-2
mutation suggests that Shp-1 and Shp-2 have antagonistic effects
in hematopoiesis, possibly through a bidirectional modulation of the
same signaling pathway(s).
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