Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

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

ABSTRACT: 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.

ORGANISM(S): Mus musculus

PROVIDER: GSE267431 | GEO | 2025/06/11

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

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

Single cell analysis of transcriptome and open chromatin reveals the dynamics of hair follicle stem cell aging [scATAC-Seq]

Project description:As the biggest organ of human body, skin and its appendages offer excellent experimental systems for aging studies. Skin wrinkling, hair greying and hair loss are among the most striking and observable traits of aging. However, the chronic changes and cell-to-cell variation accumulated during aging in different hair follicle lineages remain unexplored. Here we present a detailed analysis of scRNAseq and scATACseq data from young and aging animals. We found distinct cellular state changes of individual hair follicle populations.

2023-06-25 | GSE227783 | GEO

Single cell analysis of transcriptome and open chromatin reveals the dynamics of hair follicle stem cell aging [scRNA-Seq]

2023-06-25 | GSE227782 | GEO

Bulk and single RNA sequencing on the role of Igf2bp2 in myeloid-biased HSC

Project description:Using RNA sequencing analysis on myeloid biased HSC, we compared gene expression profiles between WT and Igf2bp2 knock-out mice at young and old age. 1421 differentially expressed genes were identified in young myeloid biased HSC from Igf2bp2 knock-out mice compared to young WT; however, only 26 differentially expressed genes were identified in old myeloid biased HSC from Igf2bp2 knock-out mice compared to old WT. Compared to young WT myeloid biased HSC, myeloid biased HSC from young Igf2bp2 knock-out exhibits reduced expression of genes involved in metabolism and translation. In addition, single cell RNA sequencing analysis of myeloid biased HSC in young wildtype mice identified nine sub-clusters. HSCs from a sub-cluster with high expression of Igf2bp2 exhibit up-regulated IGF/PI3K/AKT signaling and increased expression of genes involved in HSC quiescence and maintenance. Altogether, the study provides a correlation and mechanism to understand the role of Igf2bp2 in HSC function and aging.

2021-02-05 | GSE166176 | GEO

Oocyte developmental competence is instructed by H3.3 chaperone Hira complex

Project description:Reproductive success begins with a healthy egg (a competent oocyte). An oocyte acquires its developmental competence during oogenesis in preparation for accomplishing the critical developmental transition from completion of meiosis to initiation of early embryogenesis. Here we comprehensively characterised the maternal role of major subunits of Hira (i.e. Hira, Cabin1 and Zscan4) during oocyte-to-embryo transition.

2022-02-01 | GSE146894 | GEO

Cxxc finger protein 1 maintains homeostasis and function of intestinal group 3 innate lymphoid cells with aging [control scRNA-seq]

Project description:To investigate the role of aging in the regulation of ILC3 development and function, we used the young mice as control and carried out single-cell RNA sequencing (BD Rhapsody) on young gut ILC3s.

2023-06-07 | GSE210193 | GEO

Nucleosome loss leads to global transcriptional upregulation and genomic instability during yeast replicative aging

Project description:All eukaryotic cells divide a finite number of times, termed replicative aging, but the reason for this is not clear. Consistent with the decreased total histone protein levels in aged Saccharomyces cerevisiae, which is a cause of aging (1), we find that nucleosome occupancy decreases 50% across the whole genome during replicative aging by spike-in controlled MNase sequencing. Nucleosomes become fuzzier or move to sequences predicted to better accommodate histone octamers. All yeast genes are induced during aging. Genes that are repressed in young cells are most induced, accompanied by nucleosome loss from their promoters that have unique chromatin organization. Contrary to the loss of mitochondrial function during aging, mitochondrial DNA content increases and unprecedented levels of large-scale chromosomal alterations and increased retrotransposition are observed. Mnase-Seq experiments were carried out for young yeast, old yeast, and old yeast with histone over expression, 3 replicates were done for each category. RNA-Seq were carried out for the same categories of yeast cells but with 2 replicates for each. Genome-Seq were done for the young and old yeast with 2 replicates for each.

2014-02-26 | E-GEOD-47023 | biostudies-arrayexpress

Functional stem cell aging dictated by skin tissue microenvironment

Project description:Organismal aging in mammals is manifested with architectural alteration and functional decline of multiple organs throughout the body. In aged skin, hairs are sparse, which has led to the hypothesis that the hair follicle stem cells (HFSCs) undergo epidermal differentiation during aging. Here, we employ single cell analysis to interrogate aging-related changes in the HFSCs. Unexpectedly, HFSCs maintain their lineage fidelity and show no signs of shifting to an epidermal fate. Despite maintaining lineage identity, HFSCs do show prevalent transcriptional changes in extracellular matrix genes. Of importance, these HFSC changes are accompanied by profound architectural perturbations in the aging stem cell niche. Upon surveying the dermis from young and aged skin, we also observe age-related changes in many non-epithelial cell types, including resident immune cells, sensory neurons, arrector pili muscles, and blood vessels – all of which have been previously associated with abilities to modulate hair follicle regeneration. Consistent with both intrinsic and extrinsic alterations in stem cell: niche communications, we find that in response to skin wounding, aged HFSCs repair the epidermis, but are defective in hair follicle regeneration. Intriguingly, whereas aged dermis cannot support young HFSCs, aged HFSCs can be rescued when supported by young dermis. Together, these findings favor a model where skin tissue microenvironment plays a dominant role in dictating the molecular properties and activities of HFSCs.

2019-12-31 | GSE124901 | GEO

Determination of Nir (Noc2l) function in epidermis during mouse development by global transcriptome analysis

Project description:To investigate the role of Nir in epidermis during embryogenesis, we crossed mice harboring conditional Nir alleles with the Krt14-Cre deleter strain, which results in Cre-mediated loss of Nir selectively in epidermis. Transciptome analysis of keratinocytes obtained from control and knock-out mice at E15.5 revealed 4393 genes differentially expressed between Nir knock-out and control mice (p-value<10-2). At E17.5, we found 5673 differentially expressed genes.

2018-03-05 | GSE102277 | GEO

Epigenetic clocks reveal a rejuvenation event during embryogenesis followed by aging

Project description:The notion that germline does not age goes back to the 19th century ideas of August Weismann. However, being in a metabolically active state, germline accumulates damage and other age-related changes over time, i.e., they age. For new life to begin in the same young state, they must be rejuvenated in the offspring. Here, we developed a new multi-tissue epigenetic clock and applied it, together with other aging clocks, to track changes in biological age during mouse and human prenatal development. This analysis revealed a significant decrease in biological age, i.e. rejuvenation, during early stages of embryogenesis, followed by an increase in later stages. We further found that pluripotent stem cells do not age even after extensive passaging and that the examined epigenetic age dynamics is conserved across species. Overall, this study uncovers a natural rejuvenation event during embryogenesis and suggests that the minimal biological age (the ground zero) marks the beginning of organismal aging.

2021-05-10 | GSE171332 | GEO

OmicsDI is part of the ELIXIR infrastructure

OmicsDI is an Elixir interoperability service. Learn more ›

Tweets

OmicsDI Databases

PRIDE
PeptideAtlas
MassIVE
JPOST Repository
Physiome Model Repository

EGA
EVA
ENA
LINCS
PAXDB
Cell Collective

MetaboLights
Metabolomics Workbench
MetabolomeExpress
GNPS
BioModels
FAIRDOMHub

ArrayExpress
dbGaP
ExpressionAtlas
GEO
NODE

Information

Databases
Help
API
Contact us
Code on GitHub
Terms of use
Submit Data