Giulia Barbiera

Abstract The cerebral cortex relies on vastly different types of inhibitory neurons to compute. How this diversity emerges during development remains an open question. The rarity of individual inhibitory neuron types often leads to their underrepresentation in single-cell RNA sequencing (scRNAseq) datasets, limiting insights into their developmental trajectories. To address this problem, we developed a computational pipeline to enrich and integrate rare cell types across multiple datasets.

Highlights • PGE2 suppresses IFN I induction by activated macrophages • PGE2 targets a set of poorly permissive inflammatory gene enhancers marked by MEF2A • Loss of MEF2A causes functional inactivation of inflammatory gene enhancers • MEF2A is required for IFN I induction in response to multiple innate immune stimuli Summary Tight control of inflammatory gene expression by antagonistic environmental cues is key to ensure immune protection while preventing tissue damage.

We transplanted C57Bl/6 mice with HSC transduced with either mTie2-IFN-mirT LV (IFN mice) or mTie2-GFP-mirT LV or Mock-transduced (both used as control mice), to target IFN/GFP expression to the differentiated TIE2 + monocyte progeny, which is highly enriched in tumors15,16. As shown previously, reconstitution with mTie2-IFN-mirT LV transduced cells results in a functional multi-lineage graft, with no overt side effects11,12,13.