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Transcriptome analysis of the facial processes in Rspo2, WNT9b and Rspo2 Wnt9b double mutant mice

ABSTRACT: Transcriptome analysis of the facial processes in Rspo2, WNT9b and Rspo2 Wnt9b double mutant mice

PROVIDER: PRJNA614948 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11404810.fastq.gz	Fastqsanger.gz
	SRR11404811.fastq.gz	Fastqsanger.gz
	SRR11404812.fastq.gz	Fastqsanger.gz
	SRR11404813.fastq.gz	Fastqsanger.gz
	SRR11404814.fastq.gz	Fastqsanger.gz

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Transcriptome analysis of the facial processes in Rspo2, WNT9b and Rspo2;Wnt9b double mutant mice

Project description:Purpose: To determine transcriptome profile of the facial processes of Wnt9b, Rspo2 and double gene knockout embryos by NG RNA sequencing Method: Embryonic facial process RNA samples isolated from wild type, Rspo2, Wnt9b and Rspo2;Wnt9b double mutants in triplicate (except wild type (n=2)) at embryonic day 10.5 Results: single-end 50bp reads, 19.8 million reads - 30.7 million reads.

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Project description:The Wolffian or mesonephric duct is the embryonic primordium that gives rise to the epididymis, vas deferens and seminal vesicle. The androgen action in the Wolffian duct mesenchyme during fetal development is the predominant driver for Wolffian duct maintenance which is critical for male fertility. However, the androgen’s capability of promoting Wolffian duct maintenance was completely lost in the absence of Wnt9b in mice. In this study, we followed up with this interesting phenomenon and elucidated cellular and molecular mechanisms whereby Wnt9b facilitates Wolffian duct maintenance in male embryos. Wnt9b belongs to the WNT family of secreted proteins and is expressed in the Wolffian duct epithelium. We found that the Wolffian duct degeneration in Wnt9b-/- male embryos was accompanied with decreased cell proliferation in the epithelium but not in the mesenchyme during sexual differentiation. Wnt9b deletion did not impair testicular androgen synthesis but altered expression pattern of mesenchymal androgen receptor. The percentage of androgen receptor positive cells in the mesenchyme was significantly reduced, which can be the cause of decreased epithelial proliferation. Wnt9b actions can be transduced by both β-catenin-dependent and β-catenin-independent pathways in the context of target cells. Transcriptomic analysis of E12.5 Wnt9b+/+ and Wnt9b-/- mesonephroi revealed that expression of multiple WNT/β-catenin-target genes was reduced in the absence of Wnt9b. Deletion of mesenchymal β-catenin led to caudal Wolffian duct degeneration and cystic formation in the cranial region. Taken together, our study uncovers the important WNT9B-AR signaling axis mediating the epithelial-mesenchymal interaction in Wolffian duct development.

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Project description:Canonical Wnt signaling plays a critical role in osteoblast differentiation and bone formation and is enhanced by R-spondin (RSPO) proteins. Bone morphogenetic protein-2 (BMP2) is a clinically used osteogenic factor whose regenerative efficacy is limited by dose-dependent adverse effects. We recently identified RSPO2 as a contextual enhancer of BMP2-induced bone formation, but the transcriptional mechanisms underlying this synergy remain incompletely understood. To define the molecular basis of BMP2–RSPO2 cooperation, we performed RNA sequencing (RNA-seq) analysis of MC3T3-E1 osteoblast precursor cells treated with vehicle control, RSPO2, BMP2, or BMP2+RSPO2 for 5 days under osteogenic conditions. Transcriptomic analysis revealed distinct and overlapping gene expression programs regulated by BMP2 and RSPO2, with co-treatment inducing a unique transcriptional signature enriched for genes associated with osteoblast differentiation, Wnt signaling, and cytoskeletal regulation. These data provide mechanistic insight into how RSPO2 potentiates BMP2-induced osteogenesis and support a role for RSPO2 as a therapeutic co-factor to enhance BMP2-mediated bone regeneration.

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