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S, defects in IDPs, have been associated with tooth and bone diseases. Defects in DMP1, for example, are associated with Dentinogenesis Imperfecta type III and autosomal recessive hypophosphatemic rickets [134,135]. Although the observed phenotype may be linked to low phosphate levels and inappropriate FGF23 expression in those with aberrant DMP1, these condition were the first directly linked to
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), the two most stable variants, I54A 32 and L47Q/ L55Q 32, whose half-lives are 9-fold and more than 10-fold longer than that of the wild type, respectively, were examined in an in vitro degradation system using ClpYQ and FtsH proteases. As expected from high 32 activity in vivo (26), the purified 32 mutants were co-fractionated with core RNA polymerase like wild-type 32 using gel filtration (sup
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