Single-cell epigenomics reveals mechanisms of human cortical development : (Ziffra_2021)



Single-cell epigenomics reveals mechanisms of human cortical development



Chromatin states of the developing brain

Identifying cell-type-specific enhancers

Disease risk in the regulatory landscape

Dynamic chromatin states in neurogenesis

Area-specific chromatin states

Retinoic acid in cortical arealization

Benchmarking cerebral organoids



Cell types

Calculating gene activity scores

Fig. 1 Single-cell chromatin state atlas of the developing human brain.

Fig. 2 Dynamic changes in chromatin accessibility during human cortical neurogenesis.

Fig. 3 Areal differences in chromatin state of progenitor cells foreshadow the emergence of area-specific types of excitatory neurons.

Fig. 4 Cell type-specific differences in chromatin accessibility between cerebral organoids and the developing human brain.

Extended Data Fig. 1 Batch correction and quality control metrics for primary scATAC-seq data.

Extended Data Fig. 2 Batch Correction of primary scATAC-seq samples.

Extended Data Fig. 3 Gene activity scores correlate with cell type-specific expression of marker genes.

Extended Data Fig. 4 Annotation of primary scATAC-seq peaks.

Extended Data Fig. 5 scATAC-seq peaks overlap with previously annotated bulk ATAC-seq peaks and validated forebrain enhancers.

Extended Data Fig. 6 Enrichment and depletion of disease associated variants in scATACseq peaks.

Extended Data Fig. 7 Dynamic patterns of gene expression, chromatin accessibility, and transcription factor motif enrichment across pseudotime.

Extended Data Fig. 8 Chromatin state profiling reveals divergence of PFC and V1 excitatory lineages.

Extended Data Fig. 9 Modelling the PFC–V1 split in the developing cortex.

Extended Data Fig. 10 Comparison of organoid and primary peaks reveal significant differences in chromatin landscapes.