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First published online January 12, 2006

Journal of Cell Science 119, 203e (2006)
© The Company of Biologists Limited
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In this issue

FGFR3 pulls its SOCS up


During long-bone development, a cartilage template made by chondrocytes is gradually replaced by bone. Signalling through fibroblast growth factor receptor (FGFR) 3 is required for bone elongation and, on p. 380, Efrat Monsonego-Ornan and colleagues reveal that this is modulated by suppressors of cytokine signalling (SOCS) in chondrocytes. FGFR signalling is transduced by the mitogen-activated protein kinase (MAPK) pathway and by signal transducers and activators of transcription (STATs). The latter were first identified in cytokine signalling pathways, in which SOCS proteins modulate signalling through a negative feedback loop. The authors now show that SOCS proteins also regulate signalling through FGFR3. They find that activation of FGFR3 in chondrocytes induces expression of SOCS1 and SOCS3 and that, in a chondrocyte cell line that overexpresses SOCS1, signalling through STAT1 is attenuated and signalling through MAPK is enhanced. Thus, the authors reveal a novel interaction between SOCS proteins and FGFR3 signalling that may help to determine bone length in normal individuals and in people with inherited dwarfism syndromes.


Related articles in JCS:

Suppressors of cytokine signaling (SOCS) 1 and SOCS3 interact with and modulate fibroblast growth factor receptor signaling
Tal Ben-Zvi, Avner Yayon, Arieh Gertler, and Efrat Monsonego-Ornan
JCS 2006 119: 380-387. [Abstract] [Full Text]  




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