| Literature DB >> 24549057 |
Birgitte Bertelsen1, Linea Melchior1, Lars R Jensen2, Camilla Groth3, Birte Glenthøj4, Renata Rizzo5, Nanette Mol Debes3, Liselotte Skov3, Karen Brøndum-Nielsen6, Peristera Paschou7, Asli Silahtaroglu8, Zeynep Tümer1.
Abstract
Tourette syndrome is a neurodevelopmental disorder characterized by multiple motor and vocal tics, and the disorder is often accompanied by comorbidities such as attention-deficit hyperactivity-disorder and obsessive compulsive disorder. Tourette syndrome has a complex etiology, but the underlying environmental and genetic factors are largely unknown. IMMP2L (inner mitochondrial membrane peptidase, subunit 2) located on chromosome 7q31 is one of the genes suggested as a susceptibility factor in disease pathogenesis. Through screening of a Danish cohort comprising 188 unrelated Tourette syndrome patients for copy number variations, we identified seven patients with intragenic IMMP2L deletions (3.7%), and this frequency was significantly higher (P=0.0447) compared with a Danish control cohort (0.9%). Four of the seven deletions identified did not include any known exons of IMMP2L, but were within intron 3. These deletions were found to affect a shorter IMMP2L mRNA species with two alternative 5'-exons (one including the ATG start codon). We showed that both transcripts (long and short) were expressed in several brain regions, with a particularly high expression in cerebellum and hippocampus. The current findings give further evidence for the role of IMMP2L as a susceptibility factor in Tourette syndrome and suggest that intronic changes in disease susceptibility genes should be investigated further for presence of alternatively spliced exons.Entities:
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Year: 2014 PMID: 24549057 PMCID: PMC4200436 DOI: 10.1038/ejhg.2014.24
Source DB: PubMed Journal: Eur J Hum Genet ISSN: 1018-4813 Impact factor: 4.246