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Carbonell, J.

Publications and source records attributed to Carbonell, J..

2 recordsLinked to original sources

Three-Dimensional Epigenome Roadmap of Human B-cell Differentiation Uncovers Mechanisms of Humoral Immunity and Oncogenesis

Human B-cell differentiation underlies humoral immunity, and its disruption leads to cancer, autoimmunity, and immunodeficiencies. However, the enhancer-based regulatory mechanisms governing this process remain poorly understood. To address this gap, we generated the first three-dimensional epigenomic roadmap of human B-cell differentiation in vivo. By profiling nine differentiation stages, we linked nearly half a million enhancers to their target genes through chromatin interactions, defined their activity states, and predicted bound transcription factors. We show that the acquisition of B-cell identity, distinct from common cellular processes, relies on large enhancer networks acting additively and synergistically to finely tune transcription. We further identify a 3D epigenetic priming mechanism underlying immune memory, whereby memory B cells retain primed DNA loops that enable faster responses to antigen re-exposure. Extending this roadmap to disease, we demonstrate that B-cell malignancies preserve enhancer signatures of their cell of origin while silencing distal tumor suppressor control. Finally, we uncover a previously unappreciated oncogenic mechanism in which intragenic deletions disrupt distal gene regulation via enhancer loss. Together, this resource provides a framework for understanding the genetic and epigenetic basis of humoral immunity and immune-related diseases.

genomics↗

AraC binds the p75NTR transmembrane domain to induce neurodegeneration in mature neurons.

BackgroundCytosine arabinoside (AraC) is one of the main therapeutic treatments for several types of cancer including acute myeloid leukaemia. However, after high dose AraC chemotherapy regime, patients develop severe neurotoxicity and neurodegeneration in the central nervous system leading to cerebellar ataxia, dysarthria, nystagmus, somnolence and drowsiness. AraC induces apoptosis in dividing cells, however, the mechanism by which it leads to neurite degeneration and cell death in mature neurons remains unclear. We hypothesized that the upregulation of the death receptor p75NTR is responsible for AraC-mediated neurodegeneration and cell death in leukemia patients undergoing AraC treatment. MethodsTo determine the role of AraC-p75NTR signalling in degeneration of mature cerebellar granule neurons, we used primary cultures from p75NTR knockout and p75NTRCys259 mice. Evaluation of neurodegeneration, cell death and p75NTR signalling was done by immunohistochemistry and immunoblotting. To assess the direct interaction between AraC and p75NTR, we performed isothermal dose response-cellular thermal shift and AraTM assays as well as Homo-FRET anisotropy imaging. ResultsWe show that AraC induces neurite degeneration and programmed cell death of mature cerebellar granule neurons in a p75NTR-dependent manner. Mechanistically, AraC binds to Proline 252 and Cysteine 256 of the p75NTR transmembrane domain and selectively uncouples p75NTR from the NF{kappa}B survival pathway. This in turn, exacerbates the activation of the cell death/JNK pathway by recruitment of TRAF6 to p75NTR. ConclusionOur findings identify p75NTR as a novel molecular target to develop treatments to counteract AraC-mediated neurodegeneration.

cell biology↗