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Single cell transcriptomics reveals lineage trajectory of the retinal ganglion cells in wild-type and Atoh7-null retinas

ABSTRACT: Single cell transcriptomics reveals lineage trajectory of the retinal ganglion cells in wild-type and Atoh7-null retinas

ORGANISM(S): Mus musculus

PROVIDER: GSE149040 | GEO | 2020/11/24

REPOSITORIES: GEO

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Single cell transcriptomics reveals lineage trajectory of the retinal ganglion cells in wild-type and Atoh7-null retinas

Project description:Single cell transcriptomics reveals lineage trajectory of the retinal ganglion cells in wild-type and Atoh7-null retinas

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Single cell transcriptomics reveals lineage trajectory of retinal ganglion cells in wild-type and Atoh7-null retinas.

Project description:Atoh7 has been believed to be essential for establishing the retinal ganglion cell (RGC) lineage, and Pou4f2 and Isl1 are known to regulate RGC specification and differentiation. Here we report our further study of the roles of these transcription factors. Using bulk RNA-seq, we identify genes regulated by the three transcription factors, which expand our understanding of the scope of downstream events. Using scRNA-seq on wild-type and mutant retinal cells, we reveal a transitional cell state of retinal progenitor cells (RPCs) co-marked by Atoh7 and other genes for different lineages and shared by all early retinal lineages. We further discover the unexpected emergence of the RGC lineage in the absence of Atoh7. We conclude that competence of RPCs for different retinal fates is defined by lineage-specific genes co-expressed in the transitional state and that Atoh7 defines the RGC competence and collaborates with other factors to shepherd transitional RPCs to the RGC lineage.

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The Atoh7 shadow enhancer provides transcriptional robustness during retinal ganglion cell development

Project description:The retinal ganglion cell (RGC) competence factor ATOH7 is dynamically expressed during retinal histogenesis. ATOH7 transcription is controlled by a promoter-adjacent primary enhancer and a remote shadow enhancer (SE). Deletion of the ATOH7 human SE causes non‑syndromic congenital retinal non-attachment (NCRNA) disease, characterized by optic nerve aplasia and total blindness. We used genome editing to model NCRNA in mice. Deletion of the murine SE reduces Atoh7 mRNA >5-fold, but does not recapitulate optic nerve loss; however, SEdel/KO (knockout) trans heterozygotes have thin optic nerves. By analyzing Atoh7 mRNA and protein levels, RGC development and survival, and chromatin landscape effects, we show how the SE ensures robust Atoh7 transcriptional output. Combining SE deletion, KO and wild-type alleles in a genotypic series, we determined the amount of Atoh7 needed to produce a normal complement of adult RGCs, and the secondary consequences of graded reductions in Atoh7 dosage. Together these data reveal the workings of an evolutionary fail-safe, a duplicate enhancer mechanism hard-wired in the machinery of vertebrate retinal ganglion cell genesis.

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