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. 2005 Jul 25;1(1):e7. doi: 10.1371/journal.pgen.0010007

Table 1.

Genotype and Percentage Chimerism for the Mice Used in This Study

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aPercentage wild-type based on PCs was estimated from calculating the density of PCs in five sections at least 100 μm apart. Standard deviation is in parentheses.

bPercentage wild-type based on granule cells was estimated from counting of anti-NeuN-stained granule cells in three 65 × 65 μm regions from two sections at least 100 μm apart.

cSevere ataxia is defined as a balance beam score of two or less. Homozygous mutant ages are the average of three male and three female mice.

dThis small percentage of non-GFP PCs is likely an artifact from the thin sectioning; if a small fraction of a PC is in the section, it may not be scored GFP-positive. Examination of the same PC in the adjacent section shows that all PCs are in fact GFP-positive.

eOnly lobule X PCs were used in estimating the wild-type contribution in mutant chimeric mice sacrificed at 70 d, prior to degeneration of this lobule.

fND indicates not determined, as this mouse was sacrificed prior to developing severe ataxia.

gNM indicates not meaningful, as lobule X PCs are only a useful measure of wild-type contribution when mice are sacrificed by 70 d.

CD1, CD-1 strain (Charles River Laboratories); C57, C57BL/6J strain (Jackson Laboratory).