TY  - JOUR
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
Y1  - 2000/12/01 
JF  - Genome Research 
JO  - Genome Research 
SP  - 2006 
EP  - 2021 
DO  - 10.1101/gr.158500 
VL  - 10 
IS  - 12 
UR  - http://genome.cshlp.org/content/10/12/2006.abstract 
N2  - 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. 
ER  -