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Unbiased screening identifies TGF-β signaling and Creb5 cooperatively regulate FGF18 to control pharyngeal muscle development

ABSTRACT: Unbiased screening identifies TGF-β signaling and Creb5 cooperatively regulate FGF18 to control pharyngeal muscle development

PROVIDER: PRJNA838213 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR19214011_1.fastq.gz	Fastqsanger.gz
	SRR19214011_2.fastq.gz	Fastqsanger.gz
	SRR19214012_1.fastq.gz	Fastqsanger.gz
	SRR19214012_2.fastq.gz	Fastqsanger.gz
	SRR19214013_1.fastq.gz	Fastqsanger.gz

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Unbiased screening identifies TGF-β signaling and Creb5 cooperatively regulate FGF18 to control pharyngeal muscle development

Project description:In the present work, we investigated the mechanism that regulates perimysial-to-myogenic communication using the development of the pharyngeal muscle LVP as a model. Using unbiased single-cell RNAseq (scRNAseq) data analysis combined with mouse genetic approaches, we identified TGF-β signaling as the predominant signaling activity that enables the perimysial cells to interact with the adjacent myogenic cells during late pharyngeal muscle development. Furthermore, we identified that perimysial-specific regulator Creb5 interacts specifically with TGF-β signaling to co-activate the expression of specific perimysial-to-myogenic signals such as Fgf18 to regulate pharyngeal myogenesis. Taken together, our findings reveal that TGF-b signaling and perimysial-specific regulators may cooperatively define perimysial-to-myogenic signals in regulating pharyngeal myogenesis.

2022-12-14 | GSE203035 | GEO

TGF-β signaling and Creb5 cooperatively regulate Fgf18 to control pharyngeal muscle development.

Project description:The communication between myogenic cells and their surrounding connective tissues is indispensable for muscle morphogenesis. During late embryonic development in mice, myogenic progenitors migrate to discrete sites to form individual muscles. The detailed mechanism of this process remains unclear. Using mouse levator veli palatini (LVP) development as a model, we systematically investigated how a distinct connective tissue subpopulation, perimysial fibroblasts, communicates with myogenic cells to regulate mouse pharyngeal myogenesis. Using single-cell RNAseq data analysis, we identified that TGF-β signaling is a key regulator for the perimysial fibroblasts. Loss of TGF-β signaling in the neural crest-derived palatal mesenchyme leads to defects in perimysial fibroblasts and muscle malformation in the soft palate in Osr2Cre;Tgfbr1fl/fl mice. In particular, Creb5, a transcription factor expressed in the perimysial fibroblasts, cooperates with TGF-β signaling to activate expression of Fgf18. Moreover, Fgf18 supports pharyngeal muscle development in vivo and exogenous Fgf18 can partially rescue myogenic cell numbers in Osr2Cre;Tgfbr1fl/fl samples, illustrating that TGF-β-regulated Fgf18 signaling is required for LVP development. Collectively, our findings reveal the mechanism by which TGF-β signaling achieves its functional specificity in defining the perimysial-to-myogenic signals for pharyngeal myogenesis.

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Creb5 establishes the competence for Prg4 expression in articular cartilage

Project description:Zhang et al. identify Creb5 as a transcription factor that is required for induction of Prg4 expression by TGFbeta and EGFR ligands. They show that Creb5 directly binds to two Prg4 promoter-proximal regulatory elements, working together with a more distal regulatory element to drive induction of Prg4 by TGFbeta. These findings provide new insight into the molecular regulation of Prg4 expression in superficial zone articular chondrocytes.

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Creb5 coordinates synovial joint formation with the genesis of articular cartilage

Project description:While prior work has established that articular cartilage arises from Prg4-expressing perichondrial cells, it is not clear how this process is specifically restricted to the perichondrium of synovial joints. We document that the transcription factor Creb5 is necessary to initiate the expression of signaling molecules that both direct the formation of synovial joints and guide perichondrial tissue to form articular cartilage instead of bone. Creb5 promotes the generation of articular chondrocytes from perichondrial precursors in part by inducing expression of Wif1, which blocks a Wnt5a autoregulatory loop in the perichondrium. Postnatal deletion of Creb5 in the articular cartilage leads to loss of both flat superficial zone articular chondrocytes coupled with a loss of both Prg4 and Wif1 expression; and a non-cell autonomous up-regulation of Ctgf. Our findings indicate that Creb5 promotes both joint formation and the subsequent development of articular chondrocytes by disrupting a Wnt5a positive-feedback loop in the perichondrium.

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