RT Journal
A1 Chrast, Roman
A1 Scott, Hamish S.
A1 Papasavvas, Marie Pierre
A1 Rossier, Colette
A1 Antonarakis, Emmanuel S.
A1 Barras, Christine
A1 Davisson, Muriel T.
A1 Schmidt, Cecilia
A1 Estivill, Xavier
A1 Dierssen, Mara
A1 Pritchard, Melanie
A1 Antonarakis, Stylianos E.
T1 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
JF Genome Research 
JO Genome Research 
YR 2000 
FD December 01 
VO 10 
IS 12 
SP 2006 
OP 2021 
DO 10.1101/gr.158500 
UL http://genome.cshlp.org/content/10/12/2006.abstract 
AB 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.