Affiliations 

  • 1 Neurobiology and Genetics Group, GRMRC-Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia ; Department of Human Anatomy, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia
  • 2 Neurobiology and Genetics Group, GRMRC-Medical Genetics Laboratory, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia ; Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Obstetrics and Gynaecology, Faculty of Medicine and Health Sciences, Universiti Putra Malaysia, Selangor, Malaysia
  • 3 Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Pathology Department, The Peter MacCallum Cancer Centre, East Melbourne, Victoria, Australia
  • 4 Walter and Eliza Hall Institute of Medical Research, Victoria, Australia
  • 5 Department of Biochemistry and Molecular Biology, Monash University, Melbourne, Victoria, Australia
  • 6 Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Mathematics and Statistics, The University of Melbourne, Parkville, Victoria, Australia
  • 7 Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Department of Medical Biology, University of Melbourne, Melbourne, Victoria, Australia
  • 8 Walter and Eliza Hall Institute of Medical Research, Victoria, Australia ; Centre for Cancer Biology, University of South Australia, Department of Molecular Pathology, SA Pathology, Adelaide, Australia ; School of Molecular and Biomedical Bioscience, University of Adelaide, Adelaide, Australia ; School of Medicine, Faculty of Health Sciences, University of Adelaide, Adelaide, Australia
Genom Data, 2014 Dec;2:314-7.
PMID: 26484118 DOI: 10.1016/j.gdata.2014.09.009

Abstract

The Ts1Cje mouse model of Down syndrome (DS) has partial trisomy of mouse chromosome 16 (MMU16), which is syntenic to human chromosome 21 (HSA21). It develops various neuropathological features demonstrated by DS patients such as reduced cerebellar volume [1] and altered hippocampus-dependent learning and memory [2,3]. To understand the global gene expression effect of the partially triplicated MMU16 segment on mouse brain development, we performed the spatiotemporal transcriptome analysis of Ts1Cje and disomic control cerebral cortex, cerebellum and hippocampus harvested at four developmental time-points: postnatal day (P)1, P15, P30 and P84. Here, we provide a detailed description of the experimental and analysis procedures of the microarray dataset, which has been deposited in the Gene Expression Omnibus (GSE49050) database.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.