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Beach, K.

Publications and source records attributed to Beach, K..

2 recordsLinked to original sources

Cell-type-specific whole-genome landscape of ΔFOSB binding in nucleus accumbens after chronic cocaine exposure

The ability of neurons to respond to external stimuli involves adaptations of gene expression. The transcription factor, {Delta}FOSB, is important for the development of drug addiction, however, its gene targets have not been identified. Here we use CUT&RUN to map the genome-wide enrichment of {Delta}FOSB binding in the two major neuronal cell types of the nucleus accumbens, a key brain reward region, after cocaine exposure. The binding landscape shows that the majority of {Delta}FOSB peaks occur outside of promoter regions, including intergenic regions, and are surrounded by epigenetic marks indicative of active enhancers. BRG1, the core subunit of the SWI/SNF chromatin remodeling complex, overlaps with {Delta}FOSB peaks, consistent with earlier studies of {Delta}FOSBs interacting proteins. In addition, in silico analyses predict that {Delta}FOSB cooperatively regulates gene expression with homeobox and T-box transcription factors. These novel findings uncover key elements of {Delta}FOSBs molecular mechanisms in transcriptional regulation.

neuroscience↗

Fibroblast State Reversal By MBNL1-Dependent Transcriptome Modification Regulates Cardiac Repair

Dynamic fibroblast state transitions are responsible for the hearts fibrotic response to injury, raising the possibility that tactical control of these transitions could alter maladaptive fibrotic outcomes. Transcriptome maturation by the RNA binding protein Muscleblind Like 1 (MBNL1) has emerged as a potential driver of differentiated cell states. Here genetic lineage tracing of myofibroblasts in the injured heart demonstrated that gains in MBNL1 function corresponded to profibrotic fibroblast states. Similarly, in mice cardiac fibroblast specific MBNL1 overexpression induced a transcriptional myofibroblast profile in healthy cardiac fibroblasts that prevented the fibroproliferative phase of cardiac wound healing. By contrast loss of MBNL1 reverted cardiac fibroblasts to a pro-proliferative epicardial progenitor state that limited cardiac fibrosis following myocardial infarction. This progenitor state transition was associated with an MBNL1-dependent destabilization of the mesenchymal transition gene, Sox9. These findings suggest that MBNL1 regulation of the fibroblast transcriptome drives state transitions underlying cardiac fibrosis and repair.

cell biology↗