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Canonical Wnt/β-catenin activity and differential epigenetic marks direct sexually dimorphic regulation of Irx3 and Irx5 in developing mouse gonads

ABSTRACT: Canonical Wnt/β-catenin activity and differential epigenetic marks direct sexually dimorphic regulation of Irx3 and Irx5 in developing mouse gonads

PROVIDER: PRJNA611827 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR11284402.fastq.gz	Fastqsanger.gz
	SRR11284403.fastq.gz	Fastqsanger.gz
	SRR11284404.fastq.gz	Fastqsanger.gz
	SRR11284405.fastq.gz	Fastqsanger.gz
	SRR11284406.fastq.gz	Fastqsanger.gz

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Canonical Wnt/β-catenin activity and differential epigenetic marks direct sexually dimorphic regulation of Irx3 and Irx5 in developing mouse gonads

Project description:Irx3 and Irx5 are important for oocyte and follicle survival within the developing ovary, but their regulation had not been elucidated. Methods: XX and XY supporting cells of the gonad were FACS-purified at E13.5, and submitted to ChIP-seq for H3K27me3 and H3 as a means to normalize across cell populations. Results: We identified TCF/LEF-binding sequences within two distal enhancers of the IrxB locus that promote β-catenin responsive ovary expression. Meanwhile, Irx3 and Irx5 transcription is suppressed within the developing testis by the presence of H3K27me3 on these same sites.

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Cooperative and antagonistic roles for Irx3 and Irx5 in cardiac morphogenesis and postnatal physiology

Project description:Analysis of the roles of Irx3 and Irx5 transcription factors in mouse heart development and postnatal heart function. Results show that show that Irx3 and Irx5 have redundant function in the in the endocardium to regulate atrioventricular canal morphogenesis and outflow tract formation. A postnatal deletion of Irx3 and Irx5 surprisingly results in a restoration of the repolarization gradient that is altered in Irx5 mutant hearts, suggesting a model whereby postnatal Irx3 activity is normally repressed by Irx5. 4 genotypes were analyzed: Irx5+/- (3 samples), Irx3-/-;Irx5+/- (4 samples), Irx5-/- (3 samples), Irx5-/-;Irx3-/- (4 samples). The Irx5+/- samples are the reference.

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Tao et al. BioID of Irx3 and Irx5

Project description:This submission contains the mass spectrometry files for the manuscript by Tao et al. that describes the characterization of the two transcription factors Irx3 and Irx5 and their role in regulating sister chromatid segregation. This submission contains 8 DDA files for the following baits: BirA*-FLAG-Irx3, BirA*-FLAG-Irx5, BirA*-FLAG-GFP (control) and BirA* (control).

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Canonical Wnt/β-catenin activity and differential epigenetic marks direct sexually dimorphic regulation of Irx3 and Irx5 in developing mouse gonads.

Project description:Members of the Iroquois B (IrxB) homeodomain cluster genes, specifically Irx3 and Irx5, are crucial for heart, limb and bone development. Recently, we reported their importance for oocyte and follicle survival within the developing ovary. Irx3 and Irx5 expression begins after sex determination in the ovary but remains absent in the fetal testis. Mutually antagonistic molecular signals ensure ovary versus testis differentiation with canonical Wnt/β-catenin signals paramount for promoting the ovary pathway. Notably, few direct downstream targets have been identified. We report that Wnt/β-catenin signaling directly stimulates Irx3 and Irx5 transcription in the developing ovary. Using in silico analysis of ATAC- and ChIP-Seq databases in conjunction with mouse gonad explant transfection assays, we identified TCF/LEF-binding sequences within two distal enhancers of the IrxB locus that promote β-catenin-responsive ovary expression. Meanwhile, Irx3 and Irx5 transcription is suppressed within the developing testis by the presence of H3K27me3 on these same sites. Thus, we resolved sexually dimorphic regulation of Irx3 and Irx5 via epigenetic and β-catenin transcriptional control where their ovarian presence promotes oocyte and follicle survival vital for future ovarian health.

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