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Vol. 10, Issue 12, 2006-2021, December 2000

LETTER
The Mouse Brain Transcriptome by SAGE: Differences in Gene Expression between P30 Brains of the Partial Trisomy 16 Mouse Model of Down Syndrome (Ts65Dn) and Normals

Roman Chrast,1,2 Hamish S. Scott,1,5 Marie Pierre Papasavvas,1 Colette Rossier,1 Emmanuel S. Antonarakis,1 Christine Barras,1 Muriel T. Davisson,3 Cecilia Schmidt,3 Xavier Estivill,4 Mara Dierssen,4 Melanie Pritchard,4,6 and Stylianos E. Antonarakis1,7

1 Division of Medical Genetics and 2 Graduate Program of Cellular and Molecular Biology, Geneva University Medical School and University Hospital, Geneva, Switzerland; 3 The Jackson Laboratory, Bar Harbor, Maine 04609, USA; 4 Medical and Molecular Genetics Center, Duran i Reynals Hospital, Barcelona, Spain

Trisomy 21, or Down syndrome (DS), is the most common genetic cause of mental retardation. Changes in the neuropathology, neurochemistry, neurophysiology, and neuropharmacology of DS patients' brains indicate that there is probably abnormal development and maintenance of central nervous system structure and function. The segmental trisomy mouse (Ts65Dn) is a model of DS that shows analogous neurobehavioral defects. We have studied the global gene expression profiles of normal and Ts65Dn male and normal female mice brains (P30) using the serial analysis of gene expression (SAGE) technique. From the combined sample we collected a total of 152,791 RNA tags and observed 45,856 unique tags in the mouse brain transcriptome. There are 14 ribosomal protein genes (nine underexpressed) among the 330 statistically significant differences between normal male and Ts65Dn male brains, which possibly implies abnormal ribosomal biogenesis in the development and maintenance of DS phenotypes. This study contributes to the establishment of a mouse brain transcriptome and provides the first overall analysis of the differences in gene expression in aneuploid versus normal mammalian brain cells.

Present addresses: 5Genetics and Bioinformatics Group, Walter and Eliza Hall Institute, Royal Parade, Parkville, P.O. Royal Melbourne Hospital, Victoria 3050, Australia; 6Molecular Genetics and Development, Institute of Reproduction and Development, Monash Medical Center, Clayton 3168, Australia.

7 Corresponding author.

10:2006-2021 ©2000 by Cold Spring Harbor Laboratory Press  ISSN 1088-9051/00 $5.00
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