The development of B cells in the bone marrow decreases with increasing age. This could be related to metabolic changes resulting from defects in mitochondrial (mt) DNA, which controls OxPhos (oxidative phosphorylation). This project aims to understand how OxPhos controls the development of B cell progenitors and modulates signaling pathways in pro/pre-B cells. Therefore, we characterize B cell development in mice in which OxPhos is genetically reduced in B cells. We analyze the metabolism of developing B cells and the OxPhos dependency using metabolic single cell flow cytometry using bone marrow from different mutant mouse strains. We want to elucidate molecular pathways by which OxPhos regulates the development of progenitor B cells by metabolic pathway analysis, gene expression studies and single-cell RNA sequencing of bone marrow-derived B cells. We are also investigating potential feedback pathways, that are triggered by the disruption of OxPhos by combining genetic combining genetic experiments with pharmacological experiments in pro-B cell cultures. In summary, we aim to comprehensively understand the effects of OxPhos on B cell development.