PUBLICATION

Mutations in DCHS1 cause mitral valve prolapse

Authors
Durst, R., Sauls, K., Peal, D.S., deVlaming, A., Toomer, K., Leyne, M., Salani, M., Talkowski, M.E., Brand, H., Perrocheau, M., Simpson, C., Jett, C., Stone, M.R., Charles, F., Chiang, C., Lynch, S.N., Bouatia-Naji, N., Delling, F.N., Freed, L.A., Tribouilloy, C., Le Tourneau, T., LeMarec, H., Fernandez-Friera, L., Solis, J., Trujillano, D., Ossowski, S., Estivill, X., Dina, C., Bruneval, P., Chester, A., Schott, J.J., Irvine, K.D., Mao, Y., Wessels, A., Motiwala, T., Puceat, M., Tsukasaki, Y., Menick, D.R., Kasiganesan, H., Nie, X., Broome, A.M., Williams, K., Johnson, A., Markwald, R.R., Jeunemaitre, X., Hagege, A., Levine, R.A., Milan, D.J., Norris, R.A., Slaugenhaupt, S.A.
ID
ZDB-PUB-150811-1
Date
2015
Source
Nature   525(7567): 109-13 (Journal)
Registered Authors
Keywords
none
MeSH Terms
  • Animals
  • Body Patterning/genetics
  • Cadherins/deficiency
  • Cadherins/genetics*
  • Cadherins/metabolism*
  • Cell Movement/genetics
  • Chromosomes, Human, Pair 11/genetics
  • Female
  • Humans
  • Male
  • Mice
  • Mitral Valve/abnormalities
  • Mitral Valve/embryology
  • Mitral Valve/pathology
  • Mitral Valve/surgery
  • Mitral Valve Prolapse/genetics*
  • Mitral Valve Prolapse/pathology*
  • Mutation/genetics*
  • Pedigree
  • Phenotype
  • Protein Stability
  • RNA, Messenger/genetics
  • Zebrafish/genetics
  • Zebrafish Proteins/genetics
  • Zebrafish Proteins/metabolism
PubMed
26258302 Full text @ Nature
Abstract
Mitral valve prolapse (MVP) is a common cardiac valve disease that affects nearly 1 in 40 individuals. It can manifest as mitral regurgitation and is the leading indication for mitral valve surgery. Despite a clear heritable component, the genetic aetiology leading to non-syndromic MVP has remained elusive. Four affected individuals from a large multigenerational family segregating non-syndromic MVP underwent capture sequencing of the linked interval on chromosome 11. We report a missense mutation in the DCHS1 gene, the human homologue of the Drosophila cell polarity gene dachsous (ds), that segregates with MVP in the family. Morpholino knockdown of the zebrafish homologue dachsous1b resulted in a cardiac atrioventricular canal defect that could be rescued by wild-type human DCHS1, but not by DCHS1 messenger RNA with the familial mutation. Further genetic studies identified two additional families in which a second deleterious DCHS1 mutation segregates with MVP. Both DCHS1 mutations reduce protein stability as demonstrated in zebrafish, cultured cells and, notably, in mitral valve interstitial cells (MVICs) obtained during mitral valve repair surgery of a proband. Dchs1(+/-) mice had prolapse of thickened mitral leaflets, which could be traced back to developmental errors in valve morphogenesis. DCHS1 deficiency in MVP patient MVICs, as well as in Dchs1(+/-) mouse MVICs, result in altered migration and cellular patterning, supporting these processes as aetiological underpinnings for the disease. Understanding the role of DCHS1 in mitral valve development and MVP pathogenesis holds potential for therapeutic insights for this very common disease.
Genes / Markers
Figures
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Expression
Phenotype
Mutations / Transgenics
Human Disease / Model
Sequence Targeting Reagents
Fish
Antibodies
Orthology
Engineered Foreign Genes
Mapping