Propagation of RML Prions in Mice Expressing PrP Devoid of GPI Anchor Leads to Formation of a Novel, Stable Prion Strain
Figure 2
The cell tropism of various prion strains changes after propagation in tgGPI− mice.
Homogenates of GPI− or C57 brains infected with the strains indicated were subjected to the CPA. (A) The patterns elicited by 22L from both sources were very similar, however RML, 79A and 139A prions from wild-type brain were swa sensitive on PK1 cells and R332H11 incompetent, while those from tgGPI− brain were swa resistant and R332H1 competent. The RI600 (Response Index for 600 spots) on CAD, PK1, PK1+swa and R332H11 cells is given within the graphs (left upper corner) and the logarithm ± SD of the ratios RICAD/RIPK1 (blue) and RIPK1/RIPK1+swa (red) is plotted in the bar graph (B). The matrix (C) gives the p values for the pairwise comparison of two strains on the basis of their log[RICAD/RIPK1] (blue) and log[RIPK1/RIPK1+swa] (red) values. The framed “ns” indicates p values>0.1 for both log[ratios]. For example, C57[RML] and GPI−[RML] prions are significantly different (p = 0.0097 for log[RICAD/RIPK1] and p = 0.0001 for log[RIPK1/RIPK1+swa]), as are C57[79A] and GPI−[79A] prions, whereas C57[22L] and GPI−[22L] prions do not show a significant difference (framed “ns”; p>0.1) for both logRI ratios. By the same token C57[79A] and C57[RML], and GPI−[139A] and GPI−[RML] prions are not distinguishable, while C57[139A] and C57[RML] prions differ.