Effects of PAX5::ELN oncoprotein expression in the absence of the RAG complex. (A) Immunophenotypic characterization of bone marrow B-cell populations. UMAP of the clustering analysis of the B-cell subpopulations from 3-week- and 3-month-old mice with the indicated genotypes. The same combination of markers as in panel B was used. (B) Percentages of the medullar B-cell subpopulations, from 3-week- and 3-month-old mice with the indicated genotypes. Results are expressed as mean ± SD (GraphPad Prism) and overall differences between values were evaluated by t test with Mann–Whitney U posttest. The difference between means is significant if ∗P value <.05, very significant if ∗∗P value <.01, extremely significant if ∗∗∗P value <.001, or if ∗∗∗∗P value <.0001. (C) Kaplan-Meier survival curves. The genotypes and the numbers of mice are indicated. The follow-up and the genetic setting are as in panel A (ie, hemizygous for the PAX5::ELN–encoding cDNA insertion and homozygous for RAG2-deficiency). Note that the follow-up in Figure 1C and panel C was performed at the same time, hence the same cohorts of WT and PE mice were used as controls, the corresponding survival curves have been duplicated for the sake of clarity of the figures.
Figure 2.

Effects of PAX5::ELN oncoprotein expression in the absence of the RAG complex. (A) Immunophenotypic characterization of bone marrow B-cell populations. UMAP of the clustering analysis of the B-cell subpopulations from 3-week- and 3-month-old mice with the indicated genotypes. The same combination of markers as in panel B was used. (B) Percentages of the medullar B-cell subpopulations, from 3-week- and 3-month-old mice with the indicated genotypes. Results are expressed as mean ± SD (GraphPad Prism) and overall differences between values were evaluated by t test with Mann–Whitney U posttest. The difference between means is significant if ∗P value <.05, very significant if ∗∗P value <.01, extremely significant if ∗∗∗P value <.001, or if ∗∗∗∗P value <.0001. (C) Kaplan-Meier survival curves. The genotypes and the numbers of mice are indicated. The follow-up and the genetic setting are as in panel A (ie, hemizygous for the PAX5::ELN–encoding cDNA insertion and homozygous for RAG2-deficiency). Note that the follow-up in Figure 1C and panel C was performed at the same time, hence the same cohorts of WT and PE mice were used as controls, the corresponding survival curves have been duplicated for the sake of clarity of the figures.

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