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Thyroid hormone signaling specifies cone subtypes in human retinal organoids

ABSTRACT: Thyroid hormone signaling specifies cone subtypes in human retinal organoids

PROVIDER: PRJNA488731 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7773400.fastq.gz	Fastqsanger.gz
	SRR7773410.fastq.gz	Fastqsanger.gz
	SRR7773420.fastq.gz	Fastqsanger.gz
	SRR7773401.fastq.gz	Fastqsanger.gz
	SRR7773411.fastq.gz	Fastqsanger.gz

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Thyroid hormone signaling specifies cone subtypes in human retinal organoids

Project description:The mechanisms underlying specification of neuronal subtypes within the human nervous system are largely unknown. The blue/S, green/M and red/L cones of the retina enable high-acuity daytime and color vision. To determine the mechanism controlling S vs. L/M fates, we studied the differentiation of human retinal organoids. Organoids and retinas have similar distributions, expression profiles, and morphologies of cone subtypes. S cones are specified first, followed by L/M cones, and thyroid hormone signaling controls this temporal switch. Dynamic expression of thyroid hormone-degrading and activating proteins within the retina ensures low signaling early to specify S cones and high signaling late to produce L/M cones. This work establishes organoids as a model for determining mechanisms of human development with promising utility for therapeutics and vision repair.

2018-10-12 | GSE119320 | GEO

Transcriptional control of cone photoreceptor diversity by a thyroid hormone receptor

Project description:Purpose: To define the cone photoreceptor diversity and underlying transcriptional controls in mouse retina Methods: Individual retinal cone cells were isolated by micro-manipulator from dissociated pieces of superior/inferior retina from heterozygous (or homozygous) Thrb-b2Cre:Ai6 mice. Single cell libraries were constructed for RNA-seq analysis. Thrb-b2Cre;Rosa26-Sun1Gfp mice were used to isolate cone nuclei for ATAC-seq analysis. Thrb-HAB mice were used to identify TRb2 genomic binding sites using ChAP-seq analysis. Results: Developmental analyses of individual cones revealed a network of gradient genes. Many of these gradient genes are regulated by TRb2, a thyroid hormone receptor that has been associated with color visual impairment. Conclusions: The results suggest that TRb2 controls chromatin remodeling and transcriptional plasticity in the cone lineage to promote diversity.

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Thyroid hormone signaling specifies cone subtypes in human retinal organoids.

Project description:The mechanisms underlying specification of neuronal subtypes within the human nervous system are largely unknown. The blue (S), green (M), and red (L) cones of the retina enable high-acuity daytime and color vision. To determine the mechanism that controls S versus L/M fates, we studied the differentiation of human retinal organoids. Organoids and retinas have similar distributions, expression profiles, and morphologies of cone subtypes. S cones are specified first, followed by L/M cones, and thyroid hormone signaling controls this temporal switch. Dynamic expression of thyroid hormone-degrading and -activating proteins within the retina ensures low signaling early to specify S cones and high signaling late to produce L/M cones. This work establishes organoids as a model for determining mechanisms of human development with promising utility for therapeutics and vision repair.

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Transcriptional control of cone photoreceptor diversity by a thyroid hormone receptor

Project description:Transcriptional control of cone photoreceptor diversity by a thyroid hormone receptor

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The Circadian Clock Gene Bmal1 Controls Thyroid Hormone-Mediated Spectral Identity and Cone Photoreceptor Function

Project description:Here we reveal a novel role for the circadian clock gene Bmal1 and Period2 in regulating the spatial organization of the cone opsins. Deletion of Bmal1 and Per2 have opposing effects on S-opsin expression and patterning of the cone photoreceptors is disrupted in cone specific knockouts of these genes. Using ChIP analysis we show that BMAL1 directly binds to the promoter region of the thyroid activating enzyme type II deiodinase (Dio2).

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Thyroid hormone receptor alpha is required for thyroid hormone-dependent neural cell proliferation during tadpole metamorphosis

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