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Vol. 15, No. 2, pp. 241-253, January 15, 2001
1 Department of Pathology, University of Rochester,
Rochester, New York 14627, USA; 2 National Human Genome
Research Institute and 3 National Cancer Institute, National
Institutes of Health, Bethesda, Maryland 20892, USA
Mutant src
/ mice have osteopetrosis
resulting from defective osteoclasts, the cells that resorb bone.
However, signaling pathways involving Src family members in osteoclasts
remain unclear. We demonstrate that expression of a truncated Src
molecule, Src251, lacking the kinase domain, induces osteopetrosis in
wild-type and src+/ mice and worsens
osteopetrosis in src/ mice by a novel
mechanism, increased osteoclast apoptosis. Induction of apoptosis by
Src251 requires a functional SH2, but not an SH3, domain and is
associated with reduced AKT kinase activity. Expression of Src251
dramatically reduces osteoclast survival in response to
RANKL/TRANCE/OPGL, providing evidence that Src family kinases are
required in vivo for survival signaling pathways downstream from TNF
family receptors.
[Key Words: Src; RANK; osteoclast; apoptosis]
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