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Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [RNA-seq]

ABSTRACT: Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [RNA-seq]

PROVIDER: PRJNA936921 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR23560843_1.fastq.gz	Fastqsanger.gz
	SRR23560843_2.fastq.gz	Fastqsanger.gz
	SRR23560844_1.fastq.gz	Fastqsanger.gz
	SRR23560844_2.fastq.gz	Fastqsanger.gz
	SRR23560845_1.fastq.gz	Fastqsanger.gz

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Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [RNA-seq]

Project description:The deletion of a single miRNA cluster, miR-17~92, is sufficient to induce primary sex reversal in XY mice. The expression of the testis determining gene, Sry, is delayed in embryonic XY miR-17~92 knockout gonads, which immediately activate the ovarian genetic program. Single cell RNA-seq analysis shows that Sertoli cell differentiation is highly reduced, delayed and unable to trigger testis differentiation. Consistent with the well-known role of miRNAs in gene regulation, the expression of target genes of miR-17~92 is not stabilized in XY mutant gonads at E11.5, affecting, in turn, the fine regulation of large gene networks involved in mammalian sex determination. Our results reveal that the miR-17~92 cluster is a novel sex-determining factor that modulates several gene networks required for accurate timing of Sry expression and Sertoli cell differentiation during testis determination and early differentiation. bulk RNA-seq, single cell RNA-seq as well as IF and other characterizations of a transgenic mice for miR-17~92 cluster

2023-07-09 | GSE225675 | GEO

Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [scRNA-seq]

2023-07-09 | GSE225676 | GEO

Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster

Project description:Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster

| PRJNA936915 | ENA

Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [scRNA-seq]

Project description:Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster [scRNA-seq]

| PRJNA936922 | ENA

Differential gene expression in nephron progenitors lacking miR-17~92

2014-03-07 | GSE52514 | GEO

Differential gene expression in nephron progenitors lacking miR-17~92

Project description:Purpose: The goal of this study is to compare the differential expression of transcripts in control kidneys compared to kidneys lacking the miR-17~92 cluster in nephron progenitors and their derivatives by RNA-seq to identify potential miRNA targets in the mutant kidneys. mRNA profiles of control and mutant (=Six2-TGC; miR-17~92 flx/flx) embryonic day 16 kidneys were generated by deep sequencing, in triplicate, using Illumina HiSeq2000

2014-03-07 | E-GEOD-52514 | biostudies-arrayexpress

Complete male-to-female sex reversal in mice lacking the miR-17~92 cluster

Project description:This SuperSeries is composed of the SubSeries listed below.

2023-07-09 | GSE225677 | GEO

The transcription factor TAL1 and the miR-17-92 cluster establish a regulatory loop

Project description:A network of gene regulatory factors such as transcription factors and microRNAs establish and maintain the gene expression pattern during hematopoiesis. In this network transcription factors regulate each other and are involved in regulatory loops with microRNAs.The microRNA cluster miR-17-92 is located within the MIR17HG gene and encodes for six mature microRNAs. It is important for hematopoietic differentiation and plays a central role in malignant disease. However, the transcription factors downstream of miR-17-92 are largely elusive and the transcriptional regulation of miR-17-92 is not fully understood. Here we show that miR-17-92 forms a regulatory loop with the transcription factor TAL1. The miR-17-92 cluster inhibits expression of TAL1 and indirectly leads to decreased stability of the TAL1 transcriptional complex. We found that TAL1 and its heterodimerization partner E47 regulate miR-17-92 transcriptionally. Furthermore, miR-17-92 negatively influences erythroid differentiation, a process that depends on gene activation by the TAL1 complex. Our data give example of how transcription factor activity is fine-tuned during normal hematopoiesis. We postulate that disturbance of the regulatory loop between TAL1 and the miR-17-92 cluster could be an important step in cancer development and progression.

2021-09-09 | PXD018052 | Pride

The miR-17~92 microRNA cluster is a global regulator of tumor metabolism

Project description:mRNA expression in Eμ-Myc lymphoma cells expressing or lacking miR-17~92

2016-07-14 | GSE77010 | GEO

Control of oligodendroglial cell number by the miR-17~92 family of miRNA cluster (mRNA profiling)

Project description:The generation of myelinating cells in the central nervous system (CNS) requires the initiation of specific gene-expression programs in oligodendrocytes. We reasoned that miRNAs could play an important role in this process by regulating critical developmental genes. Microarray profiling of cultured oligodendrocytes identifies the miR-17~92 family of miRNA cluster as highly enriched miRNAs in oligodendrocytes.We specifically deleted the miR-17~92 cluster in oligodendrocytes using the 2´3´-cyclic nucleotide 3´-phosphodiesterase (CNP)-Cre mice. Absence of miR-17~92 leads to a reduction of oligodendrocyte number in vivo and we find that the expression of these miRNAs in primary cultures of oligodendrocytes promotes cell proliferation by influencing Akt signalling. Together, these results suggest that the miRNA pathway is essential in determining oligodendroglial cell number and that the miR-17~92 cluster is crucial in this process.

2010-06-01 | GSE21797 | GEO

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