Variant Synonymizer: Platform to identify mutations defined in different ways is available now!
Over 2,000 gene–disease validation summaries are now available—no login required!
Dentin sialophosphoprotein (DSPP) variants are established causes of autosomal dominant dentinogenesis imperfecta type II (Dentinogenesis imperfecta type II). A heterozygous splice-donor mutation, c.135+2T>C, was identified in a four-generation kindred with classical DGI-II features, including opalescent "shell" teeth and enlarged pulp chambers, co-segregating with disease in all affected relatives ([PMID:22125647]). No additional DSPP variants were found in unaffected family members, supporting pathogenicity.
Functional assays demonstrate that c.135+2T>C abolishes normal splicing of intron 3, resulting in aberrant exon skipping and extended DSPP transcripts in vitro ([PMID:22125647]). Complementary in vivo studies reveal that proteolytic processing of DSPP is essential for dentin mineralization: transgenic mice expressing a processing-deficient D452A-DSPP mutant fail to rescue dentin defects in Dspp-knockout backgrounds, confirming a loss-of-function mechanism ([PMID:22798071]).
Key Take-home: DSPP genetic testing, including splice-site analysis, is critical for molecular diagnosis and management of DGI-II.
Gene–Disease AssociationLimitedSingle autosomal dominant family with co-segregation of c.135+2T>C variant and DGI-II ([PMID:22125647]). Genetic EvidenceLimitedOne DGI-II pedigree with a splice-donor DSPP mutation segregating in four generations. Functional EvidenceModerateIn vitro splicing assays show exon-skipping by c.135+2T>C ([PMID:22125647]), and mouse transgenic studies confirm necessity of DSPP proteolytic processing for dentinogenesis ([PMID:22798071]). |