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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture

ABSTRACT: Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture

PROVIDER: PRJNA539934 | ENA |

REPOSITORIES: ENA

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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture [Repli-Chip]

Project description:Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture [Repli-Chip]

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Project description:Human B-lineage precursor acute lymphoid leukemias (BCP-ALLs) comprise a group of genetically and clinically distinct disease entities with features of differentiation arrest at known stages of normal B-lineage differentiation. We previously showed BCP-ALL cells display unique and clonally heritable DNA-replication timing (RT) programs; i.e., programs describing the variable order of replication and sub-nuclear 3D architecture of megabase-scale chromosomal units of DNA in different cell types. To determine the extent to which BCP-ALL RT programs mirror or deviate from specific stages of normal human B-cell differentiation, we transplanted immunodeficient mice with quiescent normal human CD34+ cord blood cells and obtained RT signatures of the regenerating B-lineage populations. We then compared these with RT signatures for leukemic cells from a large cohort of BCP-ALL patients of varied genetic subtype and outcome. The results identify BCP-ALL subtype-specific features that resemble specific stages of B-cell differentiation and features that appear associated with relapse. These results suggest the genesis of BCP-ALL involves alterations in RT that reflect biologically significant and clinically relevant leukemia-specific epigenetic changes that have potential as a novel genre of prognostic biomarkers.

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Replication timing alterations in leukemia reflect stable clinically-relevant changes in genome architecture

Project description:This SuperSeries is composed of the SubSeries listed below.

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Project description:Despite the widespread use of glucocorticoids (GCs) for treating inflammatory conditions, the underlying mechanisms of their anti-inflammatory effects are not understood. Moreover, the majority of molecular investigations have examined the effects of glucocorticoid receptor (GR) activation prior to inflammatory challenges. However, clinically relevant situations are emulated by a GC intervention initiated in the midst of rampant inflammatory responses. To characterize the effects of a late GC treatment, we performed systematic profiling of macrophage transcriptional and regulatory landscapes with Dexamethasone (Dex) treatment either before or after stimulation by lipopolysaccharide (LPS). GR activation by Dex following LPS stimulation had a similar anti-inflammatory profile in comparison to GR pre-activation, while ameliorating the disruption of metabolic genes. Unexpectedly, the chromatin occupancy pattern of GR is not predictive of the Dex-regulated expression changes and shows little evidence for the widely accepted ‘trans-repression by tethering’ model. Rather, we find that GR activation results in global blockade of NF-κB binding to chromatin. Integrative analyses of gene expression, transcription factor occupancy, and chromatin accessibility data highlight distinct mechanisms through which GR controls inflammatory macrophages: prevention of NF-κB chromatin occupancy and activation of negative regulators such as Nfkbia, Dusp1, Tnfaip3, and Tsc22d3. Our investigation with differentially timed GC treatments reveals molecular mechanisms underlying therapeutic actions of GR for modulating the ‘inflamed epigenome’.

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