Journal article
Functional transcriptome analysis of the postnatal brain of the Ts1Cje mouse model for Down syndrome reveals global disruption of interferon-related molecular networks
KH Ling, CA Hewitt, KL Tan, PS Cheah, S Vidyadaran, MI Lai, HC Lee, K Simpson, L Hyde, MA Pritchard, GK Smyth, T Thomas, HS Scott
BMC Genomics | Published : 2014
Abstract
Background: The Ts1Cje mouse model of Down syndrome (DS) has partial triplication of mouse chromosome 16 (MMU16), which is partially homologous to human chromosome 21. These mice develop various neuropathological features identified in DS individuals. We analysed the effect of partial triplication of the MMU16 segment on global gene expression in the cerebral cortex, cerebellum and hippocampus of Ts1Cje mice at 4 time-points: postnatal day (P)1, P15, P30 and P84.Results: Gene expression profiling identified a total of 317 differentially expressed genes (DEGs), selected from various spatiotemporal comparisons, between Ts1Cje and disomic mice. A total of 201 DEGs were identified from the cereb..
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Grants
Awarded by National Health and Medical Research Council
Funding Acknowledgements
This work was supported by National Health and Medical Research Council fellowships (461204 and APP1023059 to HSS); National Health and Medical Research Council Grants 219176, 257501, and 215201 (to HSS and GKS); Sciencefund Grant, MOSTI, Malaysia (02-01-04-SF1306) awarded to P-SC; and the APEX Foundation for Research into Intellectual Disability Limited to CAH: K-HL was a recipient of the Melbourne International Fee Remission Scholarship and Universiti Putra Malaysia Staff Training Scholarship, and a Adelaide Fees Scholarship International equivalent. K-LT and H-CL were a recipient of Malaysian Ministry of Higher Education MyPhD scholarship. The microarrays were performed by the Australian Genome Research Facility, which was established through the Commonwealth-funded Major National Research Facilities program. The authors would like to thank Teresa Occhiodoro for editing advice.