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Sp5 and Sp8 recruit b-catenin to the Tcf1-Lef1 enhanceosome to activate Wnt target gene transcription

ABSTRACT: Sp5 and Sp8 recruit b-catenin to the Tcf1-Lef1 enhanceosome to activate Wnt target gene transcription

PROVIDER: PRJNA296048 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR2392540.fastq.gz	Fastqsanger.gz
	SRR2392541.fastq.gz	Fastqsanger.gz
	SRR2392542.fastq.gz	Fastqsanger.gz
	SRR2392539.fastq.gz	Fastqsanger.gz
	SRR2420860_1.fastq.gz	Fastqsanger.gz

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Sp5 and Sp8 recruit b-catenin to the Tcf1-Lef1 enhanceosome to activate Wnt target gene transcription

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SP5 and SP8 transcription factors drive primary cilia formation in early embryo

Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.

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Sp5 and Sp8 recruit b-catenin to the Tcf1-Lef1 enhanceosome to activate Wnt target gene transcription

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Sp5 and Sp8 recruit β-catenin and Tcf1-Lef1 to select enhancers to activate Wnt target gene transcription.

Project description:The ancient, highly conserved, Wnt signaling pathway regulates cell fate in all metazoans. We have previously shown that combined null mutations of the specificity protein (Sp) 1/Klf-like zinc-finger transcription factors Sp5 and Sp8 (i.e., Sp5/8) result in an embryonic phenotype identical to that observed when core components of the Wnt/β-catenin pathway are mutated; however, their role in Wnt signal transduction is unknown. Here, we show in mouse embryos and differentiating embryonic stem cells that Sp5/8 are gene-specific transcriptional coactivators in the Wnt/β-catenin pathway. Sp5/8 bind directly to GC boxes in Wnt target gene enhancers and to adjacent, or distally positioned, chromatin-bound T-cell factor (Tcf) 1/lymphoid enhancer factor (Lef) 1 to facilitate recruitment of β-catenin to target gene enhancers. Because Sp5 is itself directly activated by Wnt signals, we propose that Sp5 is a Wnt/β-catenin pathway-specific transcript on factor that functions in a feed-forward loop to robustly activate select Wnt target genes.

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SP5 and SP8 transcription factors drive primary cilia formation in early embryo [scRNA-seq]

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SP5 and SP8 transcription factors drive primary cilia formation in the early embryo [ChIP-seq]

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SP5 and SP8 transcription factors drive primary cilia formation in the early embryo [ATAC-seq]

Project description:Primary cilia play critical roles in sensory and signaling functions, and their dysregulation is associated with developmental abnormalities and multi-organ diseases1,2. Despite their importance, the transcriptional regulation of primary cilia genes is unclear. Here, we employed transcriptome and mouse genetic tools to identify a master regulator of primary cilia genes. By comparing ciliated and non-ciliated cells in the early embryo using scRNA-seq and ChIP-seq, we uncovered that a wide spectrum of primary cilia genes are upregulated in ciliated cells and that SP5/8 within the SP/KLF family of transcription factors bind a core set of cilia genes. Loss- and gain-of-function assays in mouse embryos and embryonic stem cells demonstrate Sp5/8, are required for the initial formation of primary cilia in all embryonic cell types. Moreover, Sp5/8 loss compromises the formation of the more specialized motile cilia present in the embryonic node. Finally, misexpression of SP8 is sufficient to induce primary cilia formation in two unciliated cell types. Our findings demonstrate that SP5/8 are essential for cilia initiation in the embryo and sufficient to drive cilia formation in unciliated cells.

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SP5 and SP8 transcription factors drive primary cilia formation in early embryo

Project description:SP5 and SP8 transcription factors drive primary cilia formation in early embryo

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SP5 and SP8 transcription factors drive primary cilia formation in early embryo [scRNA-seq]

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