Supplementary Figure 8: PTEN contributes to phosphatase activity, but PTEN haploinsufficiency does not rescue B cell development in ZIP7 deficiency; normal PLCγ2 kinase expression in P198A-Hom cells.
From: An essential role for the Zn2+ transporter ZIP7 in B cell development
(a) Reduced phosphatase activity in B cells from PTEN-deficient PTENffMb1Cre (n=2) mice compared with wild-type Mb1Cre controls (n=4). Plots show gating on the pre-B (Fraction D) population in these animals (left panel) and reduced phosphatase activity thereof in the absence of PTEN (middle panel, red fill: PTENffMb1Cre; blue fill: PTENwtMb1Cre); quantification in right panel. Bars show means and 95% CI; n=4 PTENwtMb1Cre and 2 PTENf/fMb1Cre mice; experiment done once. (b) Mean anti-PLCγ2 antibody staining in wild-type/P198A-heterozygote (closed circles) and P198A-Hom (open circles) SWHEL immature (B220+CD43-HEL+IgM+IgD-) B cells and B220-CD43- controls; bars show means and 95% CI (n=3 mice per group, experiment done once). (c-d) B cell numbers in irradiated CD45.1+ B6 mice reconstituted with WT (open triangles), PTENf/+Mb1Cre heterozygote (open circles), P198A-Hom (filled triangles) or P198A-Hom PTENf/+Mb1Cre compound mutant BM (filled circles), gated on Hardy Fractions A-F in the BM (c) and total B220+CD19+, follicular B220+CD19+CD23+CD21+ and marginal B220+CD19+CD23-CD21++ B cells in the spleen (d). Each symbol represents an individual mouse (n= 5 chimeric mice generated per genotype). Bars show means and 95% CI.
