Compensation between FOXP transcription factors maintains proper striatal function

Ahmed, Newaz I.; Khandelwal, Nitin; Anderson, Ashley G.; Oh, Emily; Vollmer, Rachael M.; Kulkarni, Ashwinikumar; Gibson, Jay R.; Konopka, Genevieve

doi:10.1016/j.celrep.2024.114257

Cited by 2 publications

(1 citation statement)

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“…6d,e) [30][31][32] . Furthermore, the expression change of Foxp4 in the postnatal striatum is consistent with previous studies showing Foxp1 and Foxp2 retaining dominance in that region postnatally, both of which exhibit high expression in the striatum in our data set 32,33 (Fig. 1j and Extended Data Figs.…”

Section: Dbit Arp-seq Allows Molecular Deconvolution Of the Developme...supporting

confidence: 92%

Spatial dynamics of mammalian brain development and neuroinflammation by multimodal tri-omics mapping

Zhang,

Rubio Rodríguez-Kirby,

Lin

et al. 2024

Preprint

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The ability to spatially map multiple layers of the omics information over different time points allows for exploring the mechanisms driving brain development, differentiation, arealization, and alterations in disease. Herein we developed and applied spatial tri-omic sequencing technologies, DBiT ARP-seq (spatial ATAC-RNA-Protein-seq) and DBiT CTRP-seq (spatial CUT&Tag-RNA-Protein-seq) together with multiplexed immunofluorescence imaging (CODEX) to map spatial dynamic remodeling in brain development and neuroinflammation. A spatiotemporal tri-omic atlas of the mouse brain was obtained at different stages from postnatal day P0 to P21, and compared to the regions of interest in the human developing brains. Specifically, in the cortical area, we discovered temporal persistence and spatial spreading of chromatin accessibility for the layer-defining transcription factors. In corpus callosum, we observed dynamic chromatin priming of myelin genes across the subregions. Together, it suggests a role for layer specific projection neurons to coordinate axonogenesis and myelination. We further mapped the brain of a lysolecithin (LPC) neuroinflammation mouse model and observed common molecular programs in development and neuroinflammation. Microglia, exhibiting both conserved and distinct programs for inflammation and resolution, are transiently activated not only at the core of the LPC lesion, but also at distal locations presumably through neuronal circuitry. Thus, this work unveiled common and differential mechanisms in brain development and neuroinflammation, resulting in a valuable data resource to investigate brain development, function and disease.

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