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Self-organizing human neuruloids allow disease modeling in the developing ectodermal compartment

ABSTRACT: Self-organizing human neuruloids allow disease modeling in the developing ectodermal compartment

PROVIDER: PRJNA486449 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR7704707.fastq.gz	Fastqsanger.gz
	SRR7704708.fastq.gz	Fastqsanger.gz

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Self-organizing human neuruloids allow disease modeling in the developing ectodermal compartment

Project description:Harnessing the self-organizing abilities of human embryonic stem cells to mimic normal and aberrant development is a pressing challenge. Generation of highly reproducible and standardized models would allow drug screening with unprecedented accuracy. Here we report single-cell RNA-seq data (10xGenomics) of human "neuruloids". Using micro-patterned technologies we recapitulate the self-organization of the complete human embryonic ectodermal compartment during neurulation containing: neural progenitors, neural crest, sensory placode and epidermis. Single-cell transcriptomics allowed the precise molecular characterization of each cell type in a faithful model of human neurulation. Additionally, isogenic neuruloids coupled to deep neural network analysis provide a unique opportunity to model human neuropathological disorders as demonstrated for Huntignton’s disease.

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Project description:Vertebrate Hox genes are key players in the establishment of structures during the development of the main body axis. Subsequently, they play important roles either in organizing secondary axial structures such as the appendages, or during homeostasis in postnatal stages and adulthood. Here we set up to analyze their elusive function in the ectodermal compartment, using the mouse limb bud as a model. We report that the HoxC gene cluster was globally co-opted to be transcribed in the distal limb ectoderm, where it is activated following the rule of temporal colinearity. These ectodermal cells subsequently produce various keratinized organs such as nails or claws. Accordingly, deletion of the HoxC cluster led to mice lacking nails (anonychia) and also hairs (alopecia), a condition stronger than the previously reported loss of function of Hoxc13, which is causative of the ectodermal dysplasia 9 (ECTD9) syndrome in human patients. We further identified, in mammals only, two ectodermal-specific enhancers located upstream the gene cluster, which act synergistically to regulate Hoxc genes in these ectodermal organs. Deletion of these enhancers alone or in combination revealed a strong quantitative component in the regulation of these genes in the ectoderm, suggesting that these two enhancers may have evolved along with mammals to provide the level of HOXC proteins necessary for the full development of hairs and nails.

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