In humans, gain- and loss-of-function mutations of the SHP-2 protein tyrosine phosphatase cause Noonan syndrome and LEOPARD syndrome, respectively. Patients that suffer from either of these diseases have skeletal abnormalities, among other symptoms. Bauler el al. show in mice that loss of SHP-2 function causes defective skeletal morphogenesis by inhibiting bone remodelling. It is probable that similar defects underlie LEOPARD syndrome in humans, so these mice should be useful for identifying and dissecting the signalling pathways affected by SHP-2 mutations. They may also yield new information about mechanisms of bone regulation.

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