A novel splice-site mutation in ECM-1 gene in a consanguineous family with lipoid proteinosis

Exp Dermatol. 2005 Dec;14(12):891-7. doi: 10.1111/j.1600-0625.2005.00374.x.

Abstract

Lipoid proteinosis (LP) (OMIM 247100) is a rare, autosomal recessive disorder. Recent studies have shown that LP is the result of reduced expression of the extracellular matrix protein gene (ECM-1), in which loss-of-function mutations have been described. In the present report, we describe a large consanguineous family with LP. We identified a homozygous splice-site mutation in intron 1 (IVS1 + 1G-->C) in three clinically affected patients. This is the first splice-site mutation reported in LP and is the most 5' of all ECM-1 mutations described thus far. It is predicted to result in the removal of the translation initiation site, thus ablating all three known ECM-1 isoforms (ECM-1a, ECM-1b, and ECM-1c). In addition, we found a novel splicing variant that is not associated with the disease (DQ010946) and results in the generation of a short, prematurely terminating transcript. This case further emphasizes the role of ECM-1 in LP and highlights the unresolved genotype-phenotype correlation in this disease.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Adolescent
  • Amino Acid Sequence
  • Base Sequence
  • Child
  • Consanguinity*
  • Cytosine
  • DNA, Recombinant*
  • Extracellular Matrix Proteins / genetics*
  • Female
  • Guanine
  • Homozygote
  • Humans
  • Infant
  • Introns
  • Lipoid Proteinosis of Urbach and Wiethe / genetics*
  • Lipoid Proteinosis of Urbach and Wiethe / pathology
  • Male
  • Molecular Sequence Data
  • Mutation*
  • Pedigree
  • RNA

Substances

  • DNA, Recombinant
  • ECM1 protein, human
  • Extracellular Matrix Proteins
  • Guanine
  • RNA
  • Cytosine