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Kashanian, B.

Publications and source records attributed to Kashanian, B..

2 recordsLinked to original sources

Multi-omic human neural organoid cell atlas of the posterior brain

Patterning of the neural tube establishes midbrain and hindbrain structures that coordinate motor movement, process sensory input, and integrate cognitive functions. Cellular impairment within these structures underlie diverse neurological disorders, and in vitro organoid models promise inroads to understand development, model disease, and assess therapeutics. Here, we use paired single-cell transcriptome and accessible chromatin sequencing to map cell composition and regulatory mechanisms in organoid models of midbrain and hindbrain. We find that existing midbrain organoid protocols generate ventral and dorsal cell types, and cover regions including floor plate, dorsal and ventral midbrain, as well as adjacent hindbrain regions, such as cerebellum. Gene regulatory network (GRN) inference and transcription factor perturbation resolve mechanisms underlying neuronal differentiation. A single-cell multiplexed patterning screen identifies morphogen concentration and combinations that expand existing organoid models, including conditions that generate medulla glycinergic neurons and cerebellum glutamatergic subtypes. Differential abundance of cell states across screen conditions enables differentiation trajectory reconstruction from region-specific progenitors towards diverse neuron types of mid- and hindbrain, which reveals morphogen-regulon regulatory relationships underlying neuronal fate specification. Altogether, we present a single-cell multi-omic atlas and morphogen screen of human neural organoid models of the posterior brain, advancing our understanding of the co-developmental dynamics of regions within the developing human brain.

developmental biology↗

Single-cell epigenomic reconstruction of developmental trajectories in human neural organoid systems from pluripotency

Human cell type diversity emerges through a highly regulated series of fate restrictions from pluripotent progenitors. Fate restriction is orchestrated in part through epigenetic modifications at genes and regulatory elements, however it has been difficult to study these mechanisms in humans. Here, we use organoid models of the human central nervous system and establish single-cell profiling of histone modifications (H3K27ac, H3K27me3, H3K4me3) in organoid cells over a time course to reconstruct epigenomic trajectories governing cell identity acquisition from human pluripotency. We capture transitions from pluripotency through neuroepithelium, to retinal and brain region specification, as well as differentiation from progenitors to neuronal and glial terminal states. We find that switching of repressive and activating epigenetic modifications can precede and predict decisions at each stage, providing a temporal census of gene regulatory elements and transcription factors that we characterize in a gene regulatory network underlying human cerebral fate acquisition. We use transcriptome and chromatin accessibility measurements in the same cell from a human developing brain to validate this regulatory mode in a primary tissue. We show that abolishing histone 3 lysine 27 trimethylation (H3K27me3) through inhibition of the polycomb group protein Embryonic Ectoderm Development (EED) at the neuroectoderm stage disrupts fate restriction and leads to aberrant cell fate acquisition, ultimately influencing cell type composition in brain organoids. Altogether, our single-cell genome wide map of histone modifications during human neural organoid development serves as a blueprint (https://episcape.ethz.ch) to explore human cell fate decisions in normal physiology and in neurodevelopmental disorders. More broadly, this approach can be used to study human epigenomic trajectory mechanisms in any human organoid system. SummaryUnguided neural organoids reveal widespread and dynamic switching of epigenetic modifications during development and recapitulate fate restriction from pluripotency to terminally differentiated cells of the human central nervous system.

developmental biology↗