An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model-1

<p><b>Copyright information:</b></p><p>Taken from "An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model"</p><p>http://www.biomedcentral.com/1471-213X/7/131</p><p>BMC Developmental Biology 2007;7():131-131.</p><p>Published online 29 Nov 2007</p><p>PMCID:PMC2211317.</p><p></p>sed by fluorescence immunocytochemistry. Paraffin-embedded sections of wildtype (D3) and transchromosomic (47-1) tumours were stained with antibodies specific for neuronal (MAP-2), and glial (GFAP) proteins. Transchromosomic tumours contained far fewer glia and neurons than wildtype tumours. , D3 tumour at low magnification; , high magnification photo of the same D3 tumour; , 47-1 tumour at low magnification; , high magnification photo of the same 47-1 tumour

An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model-0

<p><b>Copyright information:</b></p><p>Taken from "An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model"</p><p>http://www.biomedcentral.com/1471-213X/7/131</p><p>BMC Developmental Biology 2007;7():131-131.</p><p>Published online 29 Nov 2007</p><p>PMCID:PMC2211317.</p><p></p>ffective trisomy of the gene content of the entire HSA21. D3 and 47-1 cells were cultured in an undifferentiated state, under identical conditions, and verified at the point of injection to retain an apparently intact copy of HSA21 in practically all 47-1 cells and no D3 cells [see Additional file &]. Thirty syngeneic mice were each injected subcutaneously with an identical inoculum of between 5–6.5 million 47-1 cells in the left flank, and the same number of D3 cells in the right flank. Resulting tumours were harvested 30 days post injection [experimental design see Additional file ]. , morphological classification of tissue types present in a typical pair of tumours which grew in the same mouse; D3 (left column, panels i, iii, v, vii) and 47-1 (right column, panels ii, iv, vi, viii). (i) and (ii) are representative sketches of (iii) and (iv), respectively. Note the absence of neuroectodermal tissue in the 47-1 tumour. , the average neuroectoderm contents of all D3 and 47-1 tumours, and of D3 and 47-1 tumour pairs which grew in the same mouse (paired tumours, n = 16 pairs), as determined by analysis of H&E sections by a histopathologist blinded to the origin of the tumours. , the average levels of Tubb3 mRNA expression (normalised to Gapdh mRNA levels) in all D3 and 47-1 tumours, and in D3 and 47-1 tumour pairs which grew in the same mouse, as determined by real-time quantitative RT-PCR; , the average levels of Gfap mRNA expression (normalised to Gapdh mRNA levels) in all D3 and 47-1 tumours, and in D3 and 47-1 tumour pairs which grew in the same mouse, as determined by real-time quantitative RT-PCR

An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model-3

<p><b>Copyright information:</b></p><p>Taken from "An additional human chromosome 21 causes suppression of neural fate of pluripotent mouse embryonic stem cells in a teratoma model"</p><p>http://www.biomedcentral.com/1471-213X/7/131</p><p>BMC Developmental Biology 2007;7():131-131.</p><p>Published online 29 Nov 2007</p><p>PMCID:PMC2211317.</p><p></p> tissue types in all tumours, and multiple HSA21 PCR markers were negative in the deleted regions, deletions must have occurred before any differentiation of ES cells in the tumours took place. The regions of the HSA21 gene map which are trisomic in some of the current segmental trisomy mouse models are indicated on the right by vertical lines, for comparison