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Osteogenesis imperfecta mutations in plastin 3 lead to impaired calcium regulation of actin bundling

Bone Research 2020年第3期8卷 320-332页

作者： Christopher L.schwebach Elena kudryashova Weili Zheng Matthew Orchard Harper smith Lucas A.Runyan Edward H.Egelman dmitri s.kudryashov Department of Chemistry and Biochemistry The Ohio State UniversityColumbusOH 43210USA Molecular Cellular and Developmental Biology graduate program The Ohio State UniversityColumbusOH 43210USA Department of Biochemistry and Molecular Genetics University of VirginiaCharlottesvilleVA 22908USA Biophysics graduate program The Ohio State UniversityColumbusOH 43210USA

Mutations in actin-bundling protein plastin 3(PLs3)emerged as a cause of congenital osteoporosis,but neither the role of PLs3 in bone development nor the mechanisms underlying PLs3-dependent osteoporosis are *** the over 20 identified osteoporosis-linked PLs3 mutations,we investigated all five that are expected to produce full-length *** of the mutations distorted an actin-binding loop in the second actin-binding domain of PLs3 and abolished F-actin bundling as revealed by cryo-EM reconstruction and protein interaction ***,the remaining four mutants fully retained F-actin bundling ***,they displayed defects in Ca2+sensitivity:two of the mutants lost the ability to be inhibited by Ca2+;while the other two became hypersensitive to *** group of the mutants with similar biochemical properties showed highly characteristic cellular ***-type PLs3 was distributed between lamellipodia and focal *** striking contrast,the Ca2+-hyposensitive mutants were not found at the leading edge but localized exclusively at focal adhesions/stress fibers,which displayed reinforced ***,the Ca2+-hypersensitive PLs3 mutants were restricted to lamellipodia,while chelation of Ca2+caused their redistribution to focal ***,the bundling-deficient mutant failed to co-localize with any F-actin structures in cells despite a preserved F-actin binding through a non-mutation-bearing actin-binding *** findings revealed that severe osteoporosis can be caused by a mutational disruption of the Ca2+-controlled PLs3’s cycling between adhesion complexes and the leading *** of the structural,biochemical,and cell biology insights enabled us to propose a molecular mechanism of plastin activity regulation by Ca2+.

关键词： cycling impaired striking

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