Triple A syndrome is caused by mutations in AAAS, a new WD-repeat protein gene

Publikation: Beitrag in FachzeitschriftForschungsartikelBeigetragenBegutachtung

Beitragende

  • Katrin Handschug - , Technische Universität Dresden (Autor:in)
  • Silke Sperling - , Max Planck Institut für Molekulare Genetik (Autor:in)
  • Sung Joo Kim Yoon - , Catholic University of Korea (Autor:in)
  • Steffen Hennig - , Max Planck Institut für Molekulare Genetik (Autor:in)
  • Adrian J.L. Clark - , Queen Mary University of London (Autor:in)
  • Angela Huebner - , Klinik und Poliklinik für Kinder- und Jugendmedizin, Technische Universität Dresden (Autor:in)

Abstract

The triple A syndrome (MIM 231550) is a rare autosomal recessive disorder characterized by adrenal insufficiency, achalasia and alacrima. The frequent association with a variety of neurological features may result in a severely disabling disease. We previously mapped the syndrome to a 6 cM interval on chromosome 12q13 and have now refined the critical region to 0 cM between KRT8 and D12S1651. Overlapping bacterial artificial chromosome (BAC) sequences of a high resolution BAC/P1-derived artificial chromosome (PAC) contig were screened for gene content and a novel gene encoding a 546 amino acid polypeptide was identified. In nine triple A syndrome patients eight different homozygous and compound heterozygous mutations were found in this gene, most of them leading to a truncated protein suggesting loss of function. RNA blotting experiments revealed marked expression in neuroendocrine and gastrointestinal structures, which are predominantly affected in triple A syndrome, supporting the hypothesis that mutations in this triple A syndrome gene (AAAS) are responsible for the disease. The predicted protein belongs to the family of WD repeat-containing proteins which exhibit a high degree of functional diversity including regulation of signal transduction, RNA processing and transcription.

Details

OriginalspracheEnglisch
Seiten (von - bis)283-290
Seitenumfang8
FachzeitschriftHuman molecular genetics
Jahrgang10
Ausgabenummer3
PublikationsstatusVeröffentlicht - 1 Feb. 2001
Peer-Review-StatusJa

Externe IDs

PubMed 11159947

Schlagworte