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Prolyl endopeptidase-mediated transcriptional regulation in quiescent and activated bone marrow-derived macrophages (CUT&Tag)

ABSTRACT: Prolyl endopeptidase-mediated transcriptional regulation in quiescent and activated bone marrow-derived macrophages (CUT&Tag)

PROVIDER: PRJNA878828 | ENA |

REPOSITORIES: ENA

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Prolyl endopeptidase-mediated transcriptional regulation in quiescent and activated bone marrow-derived macrophages (CUT&Tag)

Project description:Liver fibrosis, a pathogical change commonly existing in various chronic liver diseases, can ultimately develop into life-threatening liver cirrhosis, but effective antifibrotic therapy is absent due to limited understanding of fibrogenic process. The characteristic fibrotic scar in fibrosis is stiff and disorganized extracellular matrix (ECM) yielded by ECM remodeling, a pathogenic process with vigorous participation of aberrantly activated macrophages. Prolyl endopeptidase (PREP) is a dipeptidyl peptidase that possess both proteolytic and non-proteolytic functions. Using Prep knockout mouse, we found aggravated liver fibrosis in a NASH-related fibrosis murine model, as well as significantly altered transcriptome by in vitro M1/M2 polarization in primary macrophages after PREP ablation. Most importantly, a PREP-mediated direct transcriptional regulation to active cis-regulatory genomic regions was identified for the first time as a novel non-proteolytic function of PREP, based on significant nuclear localization of PREP and CUT&Tag-seq results. Among the PREP-downstream genes, Ctsb and Ctsd, genes encoding ECM remodeling-related profibrogenic cathepsin B and D respectively, were excessively expressed in PREP-ablated macrophages in vitro and in vivo. Our results indicates that PREP is a newly found transcriptional regulator in macrophage, and is a promising therapeutic target for fibrosis-related aberrant macrophage activation.

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Cut& Tag of quiescent muscle stem cells (MuSCs)

Project description:The maintenance of cell lineage and cell fate are essential for the function of adult stem cells. Despite this, the epigenetic mechanisms that regulate muscle stem cell (MuSC) identity are not well understood. In this study, we performed Cut&Tag of the activating histone marks H3K4me3 and H3K27ac on freshly isolated quiescent MuSCs and found that a large number of genes without transcription still maintained the permissive mark H3K4me3 but lacked the marker of active enhancers, H3K27ac. These genes included those that are essential for non-myogenic lineage determination. We found that many of the genes that were not transcribed but enriched for H3K4me3, were also enriched for the RE-1 binding motif, the motif recognized by the repressive transcription factor REST. Using a genetic mouse model where REST is conditionally knocked out of MuSCs, we further investigated the role of REST in the maintenance of quiescent MuSC cell identity. Investigation of the transcriptome and chromatin accessibility of WT and REST deficient MuSCs determined that the loss of REST results in the gain of expression of key genes of several non-myogenic tissues, particularly neuronal genes. Additionally, the loss of REST led to the dramatic reduction of the MuSC pool and the induction of muscle atrophy. The unstable cell identity caused by the genetic deletion of REST results in the MuSCs undergoing apoptosis and is the main driver of the observed loss of the MuSC pool. Together, the data presented in this study establishes a novel function of the transcription factor REST, where it safeguards the identity and myogenic lineage of MuSCs, through the repression of alternative lineages.

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