David Gosselin

TL;DR: It is found that distinct tissue environments drive divergent programs of gene expression by differentially activating a common enhancer repertoire and by inducing the expression of divergent secondary transcription factors that collaborate with PU.1 to establish tissue-specific enhancers.

TL;DR: The transcriptomes and DNA regulatory elements of human microglia ex vivo and in vitro in comparison to the mouse are defined and systematically relate these features to expression of genes associated with genome-wide association study (GWAS) risk alleles or exhibiting altered expression in neurodegenerative diseases and psychiatric disorders.

TL;DR: Evidence is presented that in mouse macrophages Rev-Erbs regulate target gene expression by inhibiting the functions of distal enhancers that are selected by macrophage-lineage-determining factors, thereby establishing a macrophice-specific program of repression.

TL;DR: The list of genes likely to be influenced by noncoding variants in AD is revised and expanded and the probable cell types in which they function are suggested to help better understand common genetic variation associated with brain diseases.

TL;DR: Using genome-wide approaches, expression of mutant Huntingtin (mHTT) in microglia promoted cell-autonomous pro-inflammatory transcriptional activation by increasing the expression and transcriptional activities of the myeloid lineage-determining factors PU.1 and C/EBPs.