Unknown,Transcriptomics,Genomics,Proteomics

Dataset Information

GAS1 is required for Notch-dependent facilitation of SHH signalling in forebrain development

ABSTRACT: A Gas1 knockout was made by replacing the Gas1 coding region with a LacZ gene. The ventral neuroepithelial midline of the rostral diencephalon of Gas1 wild type and mutant embryos at E10 were isolated using laser capture microdissection. In total five replicates for wild type and four replicates for Gas1 mutant embryos were analyzed. Each replicate consisted of a pool of five embryos of the respective genotype.

INSTRUMENT(S): Illumina HiSeq 4000

ORGANISM(S): Mus musculus

SUBMITTER: Daniele Sunaga-Franze

PROVIDER: E-MTAB-10207 | biostudies-arrayexpress |

REPOSITORIES: biostudies-arrayexpress

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Publications

GAS1 is required for NOTCH-dependent facilitation of SHH signaling in the ventral forebrain neuroepithelium.

Marczenke Maike M Sunaga-Franze Daniele Yumi DY Popp Oliver O Althaus Irene W IW Sauer Sascha S Mertins Philipp P Christ Annabel A Allen Benjamin L BL Willnow Thomas E TE

Development (Cambridge, England) 20211111 21

Growth arrest-specific 1 (GAS1) acts as a co-receptor to patched 1, promoting sonic hedgehog (SHH) signaling in the developing nervous system. GAS1 mutations in humans and animal models result in forebrain and craniofacial malformations, defects ascribed to a function for GAS1 in SHH signaling during early neurulation. Here, we confirm loss of SHH activity in the forebrain neuroepithelium in GAS1-deficient mice and in induced pluripotent stem cell-derived cell models of human neuroepithelial dif ...[more]

PMID: 34698766

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Dataset Information

GAS1 is required for Notch-dependent facilitation of SHH signalling in forebrain development

Publications

GAS1 is required for NOTCH-dependent facilitation of SHH signaling in the ventral forebrain neuroepithelium.

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