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Clonal evolution of pre-malignant B-cells in the absence of AID

ABSTRACT: We used microarrays to investigate gene expression changes in Aid-/- + Pax5+/- tumor cells.

ORGANISM(S): Mus musculus

PROVIDER: GSE122105 | GEO | 2018/11/03

REPOSITORIES: GEO

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Clonal evolution of pre-malignant B-cells in the absence of AID

Project description:Clonal evolution of pre-malignant B-cells in the absence of AID

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Transcription profiling of AID expressing leukemia and AID deficient leukemia in a mouse model of BCR-ABL1 ALL

Project description:Activation-Induced Cytidine Deaminase (AID) is required for somatic hypermutation and immunoglobulin (Ig) class switch recombination in germinal center B lymphocytes. Occasionally, AID targets non-Ig genes, thereby contributing to B cell lymphomagenesis. We recently reported aberrant expression of AID in BCR-ABL1-driven acute lymphoblastic leukemia (ALL). To elucidate the biological significance of aberrant AID expression, we studied loss of AID function in a murine model of BCR-ABL1 ALL. Mice transplanted with BCR-ABL1-transduced AID-/- bone marrow had prolonged survival as compared to mice transplanted with leukemia cells generated from AID+/+ bone marrow. Consistent with a causative role of AID in genetic instability, AID-/- leukemia had a decreased frequency of amplifications, deletions and a lower frequency of mutations in non-Ig genes including Pax5 and Rhoh as compared to AID+/+ leukemias. AID-/- and AID+/+ ALL cells showed a markedly distinct gene expression pattern as determined by principle component analysis, with 2,365 genes differentially expressed. In contrast to AID+/+ leukemia, AID-/- ALL cells failed to downregulate a number of tumor suppressor genes such as Rhoh, Cdkn1a (p21), and Blnk (SLP65). We conclude that AID accelerates clonal evolution in BCR-ABL1 ALL by enhancing genetic instability, aberrant somatic hypermutation, and by transcriptional inactivation of tumor suppressor genes. Experiment Overall Design: We used microarrays to detect differences in gene expression profiles between AID expressing leukemia and AID deficient leukemia

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Project description:Germinal centers (GC) are microstructures where B cells that have been activated by antigen can improve the affinity of their B cell receptors and differentiate into memory B cells (MBCs) or antibody secreting plasma cells. Here we have addressed the role of Activation Induced Deaminase (AID), which initiates somatic hypermutation and class switch recombination, in the terminal differentiation of GC B cells. By combining single cell transcriptome and immunoglobulin clonal analysis in a mouse model that traces AID-experienced cells, we have identified a novel subset of late prePB cells (L-prePB), which shares the strongest clonal relationships with PBs. Mice lacking AID have various alterations in the size and expression profiles of transcriptional clusters. We find that AID deficiency leads to a reduced proportion of L-prePB cells and severely impairs transitions between the L-prePB and the PB subsets. Thus, AID shapes the differentiation fate of GC B cells by enabling PB generation from a prePB state.

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Transcription profiling of mouse AID-GFP-positive vs AID-GFP-negative animals

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Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

Project description:Capture-C experiments on auxin treated control (E14-Tir) and Scc1-AID, Ring1b-AID, Ring1b-AID-Scc1-AID and CTCF-AID (with and without a 6-hour auxin treatment) cells.

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