INTRODUCTION

 
       Many scientists have been searchingfor the gene that causes early-onset torsion dystonia. This goal was finally reached in September of 1997. Early-onset torsion dystonia is a movement disorder, characterized by twisting muscle contractures, which usually begins in childhood. There are many different types of dystonia but early-onset dystonia represents the most severe and most common form of hereditary dystonia. Early-onset dystonia has the highest prevalence in the Ashkenazic-Jewish population and follows an autosomal mode of inheritance. Results of many previous studies have enabled researchers to refine the chromosomal location of this gene to a 150 kb region of human chromosome #9.                                 
      
          In September, 1997, a new gene was discovered and localized by the techniques of chromosome walking, exon trapping, and mutational screening by polymerase chain reaction (PCR) followed by single-stranded conformation polymorphism (SSCP) analysis. This new gene (DYT1) codes for a protein which contains an ATP-binding domain and has high homology to three mammalian genes, a nematode gene, and two other related proteins. It also is similar to the heat-shock protein/Clp protease family of proteins. The exact function of this protein has yet to be determined. Almost all cases of early-onset dystonia were found to have a unique deletion of the same glutamic acid codon in the DYT1 gene.