Abstract
The op/op mouse has a mutation in the macrophage colony-stimulating (CSF-1) gene. The phenotype of gross deficiency in the macrophage and osteoclast lineages corrects significantly with age, suggesting that other factors can substitute for CSF-1. This review examines the evidence that the op/op mouse is completely CSF-1 deficient and considers the possibility that alternative splicing within the CSF-1 gene might bypass the mutation, yielding an incompletely penetrant phenotype.

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