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Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

ABSTRACT: Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

PROVIDER: PRJNA1256837 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR33369729_1.fastq.gz	Fastqsanger.gz
	SRR33369729_2.fastq.gz	Fastqsanger.gz
	SRR33369730_1.fastq.gz	Fastqsanger.gz
	SRR33369730_2.fastq.gz	Fastqsanger.gz
	SRR33369731_1.fastq.gz	Fastqsanger.gz

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Similar Datasets

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [ATAC-seq]

Project description:Meiotic prophase I characterized by homologous recombination and synapsis is an intricate step for spermatogenesis. This process entails extensive changes to chromatin and transcription. Recent studies have revealed that prior to prophase I, accessible chromatin bound by paused Pol II at meiotic gene promoters is essential for their timely activation during later stages of prophase I. However, the factor responsible for promoting accessible chromatin at meiotic gene promoters before entry into prophase I is unknown. Here, we discovered that NFYA expressed in pre-meiotic germ cells promotes accessible chromatin at meiotic gene promoters. Concordantly, conditional germline deletion of Nfya in male mice blocks meiotic entry. Functionally, our spatial and single-cell ATAC-seq data revealed that loss of NFYA in pre-meiotic cells disrupts accessible chromatin at meiotic gene promoters. Our study identifies a pioneer role for NFYA in facilitating permissive chromatin at meiotic gene promoters before meiosis, thereby controlling the timely activation of meiotic genetic program during later meiosis.

2025-05-10 | GSE295941 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

2025-05-10 | GSE295964 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [scRNA-seq & scATAC-seq]

2025-05-10 | GSE296438 | GEO

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

| PRJNA1257271 | ENA

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis [CUT&RUN]

| PRJNA1256871 | ENA

Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at meiotic promoters in mice

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

2025-05-10 | GSE295991 | GEO

Project description:Transcription factor NFYA directs male meiotic entry by facilitating accessible chromatin at the promoters of genes expressed during meiosis

| PRJNA1254472 | ENA

Knockdowns of total NFYA and a NFYA long 3’ UTR isoform followed by RNA-seq to determine isoform-specific effects on gene expression

Project description:Alternative cleavage and polyadenylation (APA) produces multiple isoforms of the Nuclear Transcription Factor Y Subunit Alpha (NFYA) gene with variable length 3? untranslated regions (UTRs). These isoforms have been detected in HCT116 colon cancer cells via polyA-seq and northern blots, as well as colon cancer tissue RNA-seq data. NFYA is a transcription factor that may regulate cell growth and proliferation in cancer and development. To determine if there may be transcriptional regulation unique to the long 3’ UTR isoform, we conducted an siRNA knockdown in HCT116 cells specific to either the long isoform (by targeting sequence uniquely present in the longer transcript) or total NFYA mRNA (by targeting sequence shared by all long and short NFYA mRNA isoforms) followed by next generation sequencing of RNA (RNA-seq) to analyze the transcriptome.

2022-12-28 | GSE86179 | GEO

ELK1 and NFYA knockdown in MBA-MD-231 cell line

Project description:Dual-color transcriptional profiling of siRNA-transfected cells, targeting ELK1 and NFYA, versus mock-transfected cells.

2009-11-04 | GSE18849 | GEO

Transcription factor NFYa controls cardiomyocyte metabolism and proliferation during fetal heart development [Visium]

Project description:Cardiomyocytes are highly metabolic cells responsible for generating the contractile force that drives heart function. During fetal development and regeneration, these cells undergo active division but lose their proliferation activity in the adult heart. The mechanisms that coordinate their metabolism and proliferation are not fully understood. Here, we study the developmental functions of the transcription factor NFYa, which we previously identified from regenerating cardiomyocytes. We show that loss of NFYa profoundly alters cardiomyocyte composition, with a decrease in immature regenerative cells and an increase in trabecular and mature cardiomyocytes, as revealed by spatial and single-cell transcriptome analyses. NFYa-deleted cardiomyocytes exhibited reduced proliferation and impaired mitochondrial metabolism, contributing to the cardiac growth defect. NFYa acts as a transcriptional activator of mitochondrial metabolic genes as well as cell-cycle genes in cardiomyocytes through its interaction with the cofactor SP2, providing a direct link between metabolism and proliferation at the gene transcriptional level. Our study reveals a key role of NFYa in regulating cardiac growth before birth and a previously unrecognized transcriptional control mechanism of metabolic genes in the heart, and highlights the importance of mitochondrial metabolism during fetal heart development and regeneration.

2023-10-13 | GSE232962 | GEO

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