Pax5 Heterozygosity Delays BCR Expression in Preb-II Cells and Generates a Preleukemic Population

Introduction: In B-cells, PAX5 acts as an indispensable master regulator of proliferation and differentiation. In accordance, germline or somatic deregulation of PAX5 facilitates the development of B-cell precursor acute lymphoblastic leukemia (BCP-ALL). In this regard, our group has previously established a link between Pax5 and infection exposure in a Pax5+/- mouse model, recapitulating the human disease and providing an explanation for the unique age peak between 2-6 years in pediatric BCP-ALL (Martin-Lorenzo et al., Cancer Discovery, 2015). Nevertheless, the preleukemic setting mediated by reduced Pax5 levels is still poorly understood. Here, we deeply characterized the preleukemic population in Pax5+/- mice utilizing single-cell RNA Sequencing (scRNA-Seq) and multicolor flow cytometry (FACS) analyses.