Letter abstract


Nature Genetics 39, 882 - 888 (2007)
Published online: 10 June 2007 | doi:10.1038/ng2069

Mutations in the gene encoding the basal body protein RPGRIP1L, a nephrocystin-4 interactor, cause Joubert syndrome

Heleen H Arts1,8, Dan Doherty2,8, Sylvia E C van Beersum1, Melissa A Parisi2, Stef J F Letteboer1, Nicholas T Gorden2, Theo A Peters3, Tina Märker4, Krysta Voesenek1, Aileen Kartono1, Hamit Ozyurek5, Federico M Farin6, Hester Y Kroes7, Uwe Wolfrum4, Han G Brunner1, Frans P M Cremers1, Ian A Glass2, Nine V A M Knoers1 & Ronald Roepman1

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Protein-protein interaction analyses have uncovered a ciliary and basal body protein network that, when disrupted, can result in nephronophthisis (NPHP), Leber congenital amaurosis, Senior-Løken syndrome (SLSN) or Joubert syndrome (JBTS)1, 2, 3, 4, 5, 6. However, details of the molecular mechanisms underlying these disorders remain poorly understood. RPGRIP1-like protein (RPGRIP1L) is a homolog of RPGRIP1 (RPGR-interacting protein 1), a ciliary protein defective in Leber congenital amaurosis7, 8. We show that RPGRIP1L interacts with nephrocystin-4 and that mutations in the gene encoding nephrocystin-4 (NPHP4) that are known to cause SLSN disrupt this interaction. RPGRIP1L is ubiquitously expressed, and its protein product localizes to basal bodies. Therefore, we analyzed RPGRIP1L as a candidate gene for JBTS and identified loss-of-function mutations in three families with typical JBTS, including the characteristic mid-hindbrain malformation. This work identifies RPGRIP1L as a gene responsible for JBTS and establishes a central role for cilia and basal bodies in the pathophysiology of this disorder.

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  1. Department of Human Genetics, Radboud University Nijmegen Medical Centre and Nijmegen Centre for Molecular Life Sciences, 6500 HB Nijmegen, The Netherlands.
  2. Department of Pediatrics, University of Washington School of Medicine, Seattle, Washington 98195-6320, USA.
  3. Department of Otorhinolaryngology, Radboud University Nijmegen Medical Centre, 6500 HB Nijmegen, The Netherlands.
  4. Institut für Zoologie, Johannes Gutenberg University, D-55099 Mainz, Germany.
  5. Department of Pediatrics, Ondokuz Mayis University, 55139 Kurupelit/Samsun, Turkey.
  6. Department of Environmental and Occupational Health Sciences, School of Public Health, University of Washington, Seattle, Washington 98195-7234, USA.
  7. Division of Biomedical Genetics, University Medical Center Utrecht, 3508 AB Utrecht, The Netherlands.
  8. These authors contributed equally to this work.

Correspondence to: Ronald Roepman1 e-mail: r.roepman@antrg.umcn.nl

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