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Biology subjects

Dietz, H. C.

Publications and source records attributed to Dietz, H. C..

4 recordsLinked to original sources

Accurate assignment of disease liability to genetic variants using only population data

PurposeThe growing size of public variant repositories prompted us to test the accuracy of predicting pathogenicity of DNA variants using population data alone. MethodsUnder the a priori assumption that the ratio of the prevalence of variants in healthy and affected populations form two distinct distributions (pathogenic and benign), we used a Bayesian method to assign probability of a variant belonging to either distribution. ResultsThe approach, termed BayPR, accurately parsed 300 of 313 expertly curated cystic fibrosis transmembrane conductance regulator (CFTR) variants: 284 of 296 pathogenic/likely pathogenic (P/LP) variants in one distribution and 16 of 17 benign/likely benign (B/LB) variants in another. BayPR produced an area under the receiver operating curve (AUC) of 0.99 for 103 functionally-confirmed missense CFTR variants, equal to or exceeding ten commonly used algorithms (AUC range: 0.54 to 0.99). Application of BayPR to expertly curated variants in eight genes associated with seven Mendelian conditions assigned [≥]80% disease-causing probability to 1,350 of 1,374 (98.3%) P/LP variants and [≤]20% to 22 of 23 (95.7%) B/LB variants. ConclusionAgnostic to variant type or functional effect, BayPR provides probabilities of pathogenicity for DNA variants responsible for Mendelian disorders using only variant counts in affected and unaffected population samples.

genetics↗

Epigenetic modulation in the pathogenesis and treatment of inherited aortic aneurysm conditions

Shprintzen-Goldberg syndrome (SGS) is a rare systemic connective tissue disorder characterized by craniofacial, skeletal, neurodevelopmental, cutaneous, and cardiovascular manifestations, including aortic root aneurysm. It has significant phenotypic overlap with both Marfan syndrome (MFS) and Loeys-Dietz syndrome (LDS). We previously reported that SGS is caused by heterozygous mutations in the Sloan-Kettering Institute proto-oncogene (SKI), which encodes a potent suppressor of transforming growth factor beta (TGF{beta}) target gene expression. Herein, we show that mouse lines harboring orthologous amino acid substitutions in Ski recapitulate multiple human SGS phenotypic manifestations, including skin collagen deposition, skeletal kyphosis, behavioral hypoactivity, and aortic root aneurysm. Furthermore, aortic root aneurysm in SGS mice is associated with both increased acetylation of histone H3 at lysine-27 (H3K27) and TGF{beta} target gene expression, all of which can be ameliorated by pharmacological CBP/P300 inhibition in vivo; similar findings were seen in cultured dermal fibroblast from SGS patients. Aortic root growth is also abrogated in a mouse model of MFS by selective CBP/P300 inhibition in association with blunted expression of TGF{beta} target genes. These data document excessive H3K27 acetylation and hence TGF{beta} target gene expression in the pathogenesis of inherited presentations of aortic root aneurysm and the therapeutic potential of pharmacological epigenetic modulation.

genetics↗

Targetable cellular signaling events drive arterial rupture in knock-in mouse models of vascular Ehlers-Danlos Syndrome

Introduction Introduction Main Methods Author contributions Competing Interests Data availability References Vascular Ehlers-Danlos Syndrome (vEDS) is an autosomal-dominant connective tissue disorder caused by heterozygous mutations in the COL3A1 gene1. Currently, loss of structural integrity of the extracellular matrix is believed to drive the signs and symptoms of this condition, including spontaneous arterial dissection and/or rupture, the major cause of mortality2-4.\n\nUsing novel mouse models of vEDS that carry heterozygous Col3a1 glycine substitutions, we show that signaling abnormalities in the PLC/IP3/PKC/ERK pathway (Phospholipase C/Inositol 1,4,5-triphosphate/Protein Kinase C/Extrace ...

genetics↗

A positively selected, common, missense variant in FBN1 confers a 2.2 centimeter reduction of height in the Peruvian population

Peruvians are among the shortest people in the world. To understand the genetic basis of short stature in Peru, we examined an ethnically diverse group of Peruvians and identified a novel, population-specific, missense variant in FBN1 (E1297G) that is significantly associated with lower height in the Peruvian population. Each copy of the minor allele (frequency = 4.7%) reduces height by 2.2 cm (4.4 cm in homozygous individuals). This is the largest effect size known for a common height-associated variant. This variant shows strong evidence of positive selection within the Peruvian population and is significantly more frequent in Native American populations from coastal regions of Peru compared to populations from the Andes or the Amazon, suggesting that short stature in Peruvians is the result of adaptation to the coastal environment. One Sentence SummaryA mutation found in Peruvians has the largest known effect on height for a common variant. This variant is specific to Native American ancestry.

genomics↗