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. 2022 Mar 23;11(4):415–433. doi: 10.1093/stcltm/szac008

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© The Author(s) 2022. Published by Oxford University Press.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (https://creativecommons.org/licenses/by/4.0/), which permits unrestricted reuse, distribution, and reproduction in any medium, provided the original work is properly cited.

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Figure 4. — Single-cell RNA-Seq reveals the presence of retinoma and Rb cells in H9 RB1-null organoids. (A, B) UMAPs showing the cell clusters in control and RB1-null hESC organoids (A) and cell cycle distribution (B). (C) UMAP of integrated control and H9 RB1-null hESC organoids with cell cluster annotations. (D) Expression of key retinal cell type markers genes used to facilitate cluster definition in C overlaid onto the UMAPs. (E) Percentages of cells in each cell cluster of control and RB1-null hESC organoids. (F) Monocle-2 pseudotime showing progression from UPRCs to retinoma and Rb cell clusters. Cluster 11 was exempted from analysis because of low read number. RPCs: retinal progenitor cells, MGs: Müller glia cells, NRPCs: neurogenic RPCs, RGCs: retinal ganglion cells, UPRCs: cones with high expression of genes involved in unfolded protein response, RGCP: RGC precursor, T1, T2, T3: transient neurogenic progenitor populations.