This phenotype segregated with a monoallelic mutation in ATP6V1H. Since osteoporosis is the opposite of the osteopetrosis seen in Atp6i-deficient mice and expected for reduced V-ATPase activity, we studied the phenotype of zebrafish harboring a null mutation in atp6v1h. Indeed, this animal model displayed reduced bone mass, and we demonstrated that the bone defect was mediated by increased activity of mmp9 and mmp13. Here, MMP9 is linked to osteoporosis.