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Blood, Vol. 113, Issue 9, 1929-1937, February 26, 2009
Hematopoietic defects in the Ts1Cje mouse model of Down syndrome
Blood Carmichael et al.
113: 1929
Supplemental materials for: Carmichael et al
Files in this Data Supplement:
- Table S1. Triplicated genes in the Ts1Cje and Ts65Dn mouse models of DS (PDF, 4.19 MB) -
All known genes located between Mrpl39 and Zfp295 (Ts65Dn) and Sod1 and Zfp295 (Ts1Cje) are shown (UCSC mouse genome browser Feb 2006 version). The region of overlap between the two mouse models is shown, as well as the distinct region triplicated only in the Ts65Dn mouse model.
- Table S2. Peripheral blood red cell and platelet data (PDF, 466 KB) -
Average blood cell counts for red cell parameters and platelet counts for 1, 3, 6, and 10 month old disomic and Ts1Cje mice.
- Table S3. Haematopoietic phenotypes of Ts65Dn and Ts1Cje mice (PDF, 815 KB) -
All haematopoietic abnormalities that have been deteremined by Kirsammer et al in the Ts65Dn mice, and by Carmichael et al in the current manuscript in the Ts1Cje mice have been summarised. This table demonstrates the overlapping phenotypes as well as the distinct differences between the two mouse models.
- Table S4. Histological analysis of aged Ts1Cje and Gata1Plt13 mice (PDF, 218 KB) -
Three independent ageing cohorts were established to determine the effect of Ts1Cje trisomic segment and/or the Gata1Plt13 mutation on aged mice. The genetic background was either Balb/c (B) or C57BL/6:Balb/c (F1). Gata1Plt13/+ mice were crossed with the Ts1Cje model of partial trisomy. Cohort sizes (n) ranged from 9–30 mice. Mice were analysed when they became sick or moribund and a histological survey was performed. The experiment was terminated after two years for the Balb/c cohort, and at 500 days for the Ts1 cohort. Histology was assessed for the presence of bone overgrowth, lymphoid leukaemia, reticulum cell sarcoma (RCS), polycystic kidneys and lung adenoma. A percentage value is shown, which represents the frequency of each condition amongst mice for which a histological survey was performed.
- Figure S1. Peripheral blood abnormalities in Ts1Cje mice are intrinsic to the bone marrow (JPG, 65.9 KB)
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The peripheral blood abnormalities in the Ts1Cje mice can be transplanted into recipient mice through BM reconstitution. BM from four donor mice of each genotype were transplanted into two recipients each. Significance * p<0.05 ** p<0.01 *** p<0.001. Error bars are SEM.
- Figure S2. Peripheral blood abnormalities in Ts1Cje mice are still evident on a mixed C57BL/6 × Balb/c background (JPG, 63.6 KB)
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The mixed C57BL/6 × Balb/c background does not affect the peripheral blood abnormalities, or platelet count, observed in the Ts1Cje mice on a pure C57BL/6 background. When these mice are crossed to the Gata1Plt13 mice the macrocytosis and anemia are exacerbated, suggesting an additive effect of the Gata1Plt13 mutation and the trisomic segment in the Ts1Cje mice. Mice were analysed at seven weeks of age. Significance * p<0.05 ** p<0.01 *** p<0.001.
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