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Expression of GAD67 and Novel GAD67 Splice Variants During Human Fetal Pancreas Development
Authors:Esther Korpershoek  Aart M. Verwest  Ynske IJzendoorn  Robbert Rottier  Hemmo A. Drexhage  Ronald R. de Krijger
Affiliation:(1) Department of Pathology, Josephine Nefkens Institute, Room 222, Erasmus MC–University Medical Centre Rotterdam, P.O. Box 2040, Dr. Molenwaterplein 50, 3000 CA Rotterdam, The Netherlands;(2) Department of Paediatrics, Erasmus MC–Sophia, Dr. Molenwaterplein 50, Rotterdam, The Netherlands;(3) Department of Paediatric Surgery and Cell Biology and Genetics, Erasmus MC–Sophia, Dr. Molenwaterplein 50, Rotterdam, The Netherlands;(4) Department of Immunology, Erasmus MC–University Medical Centre Rotterdam, Dr. Molenwaterplein 50, Rotterdam, The Netherlands
Abstract:
Glutamic acid decarboxylase (GAD) is a major inhibitory neurotransmitter in the brain, which catalyses the reaction of l-glutamate to γ-aminobutyric acid. There are two isoforms of GAD, a 65-kDa form and a 67-kDa form, which are encoded by two different genes. As previous studies suggested a role for GAD67 splice variants during fetal pancreas development, we have investigated the mRNA expression of GAD67 and GAD67 splice variants in a series of 14 human fetal pancreases between 14 weeks gestation and term and in adult control pancreases by RT-PCR. In this study, we demonstrate mRNA expression of GAD67 and four GAD67 splice variants, including GAD25, in human fetal and adult specimens. Some of the splice variants, including various proportions of exon 7 or a new exon between exons 6 and 7, have not been described before in the human pancreas. We speculate that the expression of these GAD67 splice variants might be related to human fetal pancreas development.
Keywords:fetal development   GAD   pancreas  alternative splicing  human development
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