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Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (ATAC-Seq)

ABSTRACT: Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (ATAC-Seq)

PROVIDER: PRJNA1111508 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR29021935_1.fastq.gz	Fastqsanger.gz
	SRR29021935_2.fastq.gz	Fastqsanger.gz
	SRR29021936_1.fastq.gz	Fastqsanger.gz
	SRR29021936_2.fastq.gz	Fastqsanger.gz
	SRR29021937_1.fastq.gz	Fastqsanger.gz

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Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells

Project description:Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells

| PRJNA1111497 | ENA

Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (RNA-Seq)

Project description:Evidence indicates that the integrity of in utero embryonic development can influence late life healthy or unhealthy aging. However, specific links between embryonic development and late life aging are not well defined. Histone chaperone HIRA is thought to play a role in both early development and aging. Here, we explore the relationship between HIRA’s roles in development and aging by comparing lineage-specific constitutive and conditional Hira knock out in the murine pigmentary system, with constitutive knock out initiated during embryogenesis and conditional knock out in young adults. Embryonic Hira knockout leads to reduced melanoblast numbers during embryogenesis but wild type numbers of differentiated melanocytes at birth, normally functioning juvenile and young adult melanocyte stem cells (McSCs), and only a very mildly hypopigmented first hair coat. However, on closer analysis of these mice, Hira knockout melanocytic cells of newborn mice exhibit molecular markers characteristic of cell aging and proliferative deficits. As they age, mice with Hira knock out initiated during embryogenesis display marked defects in McSC maintenance and premature hair graying. Importantly, these defects are only observed when HIRA is inactivated during embryogenesis, but not in young adults. This genetic model shows that HIRA function during early development lays a foundation for subsequent maintenance of adult tissue specific stem cells during aging.

2025-06-11 | GSE267432 | GEO

Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (ATAC-Seq)

2025-06-11 | GSE267431 | GEO

Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (RNA-Seq)

Project description:Inactivation of histone chaperone HIRA unmasks a link between normal embryonic development of melanoblasts and maintenance of adult melanocyte stem cells (RNA-Seq)

| PRJNA1111507 | ENA

Transcription profiling of hip1::ura4+ and slm9::ura4+ S. pombe to investigate the role of the HIRA histone chaperone complex

Project description:The assembly of nucleosomes by histone chaperones is an important component of transcriptional regulation. Here we have assessed the global roles of the S. pombe HIRA histone chaperone complex. Microarray analysis indicates that inactivation of the HIRA complex results in increased expression of at least 4% of fission yeast genes. HIRA-regulated genes overlap with those which are normally repressed in vegetatively growing cells, such as targets of the Clr6 histone deacetylase and silenced genes located in subtelomeric regions. HIRA is also required for silencing of all 13 intact copies of the Tf2 long terminal repeat (LTR) retrotransposon. However, the role of HIRA is not restricted to bona fide promoters, because it also suppresses non-coding transcripts from solo LTR elements and spurious antisense transcripts from cryptic promoters associated with transcribed regions. Furthermore, the HIRA complex is essential in the absence of the quality control provided by nuclear exosome-mediated degradation of illegitimate transcripts. This suggests that HIRA restricts genomic accessibility, and, consistent with this, the chromosomes of cells lacking HIRA are more susceptible to genotoxic agents that cause double strand breaks. Thus the HIRA histone chaperone is required to maintain the protective functions of chromatin.

2009-07-22 | E-MTAB-130 | biostudies-arrayexpress

Histone chaperone HIRA orchestrates H4K16ac-decorated dynamic chromatin in senescent cells and is required for suppression of oncogene-induced neoplasia.

Project description:Cellular senescence is a stable proliferation arrest that suppresses tumorigenesis. Histone chaperone HIRA deposits nucleosome-destabilizing histone variant H3.3 into chromatin in a DNA replication-independent manner. Histone H3.3 and a subset of other typically M-bM-^@M-^\replication-dependentM-bM-^@M-^] core histones were expressed in non-proliferating senescent cells, the latter linked to alternative mRNA splicing and polyadenylation. Senescent cells incorporated newly-synthesized histones into chromatin, partially dependent on HIRA. HIRA and newly-deposited histone H3.3 co-localized at promoters of expressed genes, and their distribution shifted between proliferating and senescent cells, paralleling changes in gene expression. In senescent cells, gene promoters showed exceptional enrichment of a histone acetylation linked to open and dynamic chromatin, H4K16ac. Abundance of H4K16ac depended on HIRA. In the mouse, inactivation of HIRA downregulated H4K16ac and dramatically enhanced oncogene-induced hyperplasia. To conclude, HIRA controls a previously undefined dynamic non-canonical H4K16ac-decorated chromatin landscape in senescence, and also plays an unanticipated role in suppression of oncogene-induced neoplasia. Examination of HIRA protein binding alongside histone modification H4K16ac and H3.3 in proliferating and senescent IMR90 cells

2014-11-26 | E-GEOD-56307 | biostudies-arrayexpress

Cellular quiescence is dependent upon the HIRA histone chaperone

Project description:Quiescence (G0) is a reversible non-dividing state that facilitates cellular survival in adverse conditions. Here we demonstrate that the function of the HIRA histone chaperone complex is required for viability during nitrogen-starvation induced quiescence in Schizosaccharomyces pombe. G0 cells lacking the HIRA protein, Hip1 exhibit elevated levels of antisense ncRNAs and an increase in unrepaired DNA double strand breaks. Nitrogen-starved hip1∆ cells retain metabolic activity but, in contrast to wild type, rapidly lose the ability to resume proliferation. After a short period in G0 (1 day), hip1∆ mutants are able to resume cell growth in response to the restoration of a nitrogen source, but do not efficiently induce Start-specific gene expression and re-enter the cell cycle. However, hip1∆ cells rapidly progress to an unresponsive state and by 4 days in G0, the majority no longer initiate growth following nitrogen source restoration. Analysis using a conditional hip1 allele is consistent with these findings and indicates that HIRA is required for efficient exit from quiescence and prevents a permanent cell cycle arrest.

2023-11-13 | GSE129599 | GEO

Genome-wide maps of chromatin state for HIRA, UBN1 and ASF1a

Project description:The HIRA chaperone complex, comprised of HIRA, UBN1 and CABIN1, collaborates with histone-binding protein ASF1a to incorporate histone variant H3.3 into chromatin in a DNA replication-independent manner. To better understand its function and mechanism, we integrated HIRA, UBN1, ASF1a and histone H3.3 ChIP-seq and gene expression analyses. Most HIRA-binding sites co-localize with UBN1, ASF1a and H3.3 at active promoters and active and weak/poised enhancers. At promoters, binding of HIRA/UBN1/ASF1a correlates with the level of gene expression. HIRA is required for deposition of histone H3.3 at its binding sites. There are marked differences in nucleosome and co-regulator composition at different classes of HIRA-bound regulatory site. Underscoring this, we report novel physical interactions between the HIRA complex and transcription factors, a chromatin insulator and an ATP-dependent chromatin-remodelling complex. Our results map the distribution of the HIRA chaperone across the chromatin landscape and point to different interacting partners at functionally distinct regulatory sites. Examination of 3 histone chaperone proteins in HeLa cells

2013-04-18 | E-GEOD-45024 | biostudies-arrayexpress

Expression data from Control and HIRA knockdown cells

Project description:The HIRA chaperone complex, comprised of HIRA, UBN1 and CABIN1, collaborates with histone-binding protein ASF1a to incorporate histone variant H3.3 into chromatin in a DNA replication-independent manner. To better understand its function and mechanism, we integrated HIRA, UBN1, ASF1a and histone H3.3 ChIP-seq and gene expression analyses. Most HIRA-binding sites co-localize with UBN1, ASF1a and H3.3 at active promoters and active and weak/poised enhancers. At promoters, binding of HIRA/UBN1/ASF1a correlates with the level of gene expression. HIRA is required for deposition of histone H3.3 at its binding sites. There are marked differences in nucleosome and co-regulator composition at different classes of HIRA-bound regulatory site. Underscoring this, we report novel physical interactions between the HIRA complex and transcription factors, a chromatin insulator and an ATP-dependent chromatin-remodelling complex. Our results map the distribution of the HIRA chaperone across the chromatin landscape and point to different interacting partners at functionally distinct regulatory sites. We used microarrays to detail the global programme of gene expression after knockdown of HIRA HeLa cells were nucleofacted with Dharmacon control siRNA and siRNA to HIRA and RNA was isolated 72 hours after transfection in four biological replicates

2013-04-18 | E-GEOD-45022 | biostudies-arrayexpress

Cellular quiescence is dependent upon the HIRA histone chaperone

Project description:Cellular quiescence is dependent upon the HIRA histone chaperone

| PRJNA531915 | ENA