Browse
Submit Data
Databases
API
Help

Dataset Information

0 Views

0 Connections

0 Citations

0 Reanalyses

0 Downloads

Omics score: 0

Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [Nanostring]

ABSTRACT: Aging is a time-dependent biological phenomenon governed by complex networks of regulatory components and their transitions over lifetime. Yet, there have been limited efforts to pin down age-associated networks and map their dynamic characteristics onto aging phenotypes. Here, we built time-course genetic regulatory networks of NAM/ATAF/CUC (NAC) transcription factors during the course of leaf aging in Arabidopsis, using causal regulatory relationships among NACs identified from mutants of 49 aging-associated NACs. These temporal networks revealed a regulatory inversion from activating to repressive regulatory modes at a pre-senescent stage. The inversion was governed by three hub NACs, and their mutants conferred earlier aging with altered expression of reactive oxygen species and salicylic acid response genes. Overexpression of the hub NACs delayed the regulatory inversion, rendering delayed age-dependent cell death. We conclude that the regulatory inversion in NAC networks at a pre-senescent stage directs when age-dependent cell death should proceed in plants.

ORGANISM(S): Arabidopsis thaliana

PROVIDER: GSE92369 | GEO | 2018/04/29

REPOSITORIES: GEO

ACCESS DATA

Json Xml

Dataset's files

Source:

			Action	DRS
		Other

Items per page:

1 - 1 of 1

Similar Datasets

Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [RNA-Seq]

Project description:Aging is a time-dependent biological phenomenon governed by complex networks of regulatory components and their transitions over lifetime. Yet, there have been limited efforts to pin down age-associated networks and map their dynamic characteristics onto aging phenotypes. Here, we built time-course genetic regulatory networks of NAM/ATAF/CUC (NAC) transcription factors during the course of leaf aging in Arabidopsis, using causal regulatory relationships among NACs identified from mutants of 49 aging-associated NACs. These temporal networks revealed a regulatory inversion from activating to repressive regulatory modes at a pre-senescent stage. The inversion was governed by three hub NACs, and their mutants conferred earlier aging with altered expression of reactive oxygen species and salicylic acid response genes. Overexpression of the hub NACs delayed the regulatory inversion, rendering delayed age-dependent cell death. We conclude that the regulatory inversion in NAC networks at a pre-senescent stage directs when age-dependent cell death should proceed in plants.

2018-04-29 | GSE92314 | GEO

E-GEOD-92314

Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [RNA-Seq]

2020-04-15 | E-GEOD-92314 | ExpressionAtlas

Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants

Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants

| PRJNA357453 | ENA

Arabidopsis thaliana

Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [Nanostring]

| PRJNA357454 | ENA

Arabidopsis thaliana

Project description:Regulatory inversion in NAC networks steers the timing of age-dependent cell death in plants [RNA-Seq]

| PRJNA357201 | ENA

Single Nuclei Sequencing of old and young mice hearts under senolytica (Ageing impairs the neuro-vascular interface in the heart)

Project description:Aging is a major risk factor for impaired cardiovascular health. The aging myocardium is characterized by microcirculatory and diastolic dysfunction and increased susceptibility to arrhythmias. Nerves align with vessels during development. However, the impact of aging on the cardiac neuro-vascular interface is entirely unknown. Here, we report that aging reduces nerve density specifically in the left ventricle and dysregulates vascular-derived neuro-regulatory genes. Aging leads to a down-regulation of miR-145 and de-repression of the neuro-repulsive factor Semaphorin-3A. miR-145 deletion, which increased Sema3a expression, or endothelial Sema3a overexpression reduced axon density, thus mimicking the observed aged heart phenotype. Removal of senescent cells, which accumulated with chronological age in parallel to the decline in nerve density, rescued age-induced denervation, reduced Sema3a expression, preserved heart rate variability and reduced electrical instability. These data suggest that senescence-associated regulation of neuro-regulatory genes is associated with reduced nerve density and, thereby, contributes to age-associated cardiac dysfunction.

2023-07-05 | E-MTAB-13093 | biostudies-arrayexpress

Impaired immune surveillance accelerates accumulation of senescent cells and aging [RNA-seq]

Project description:Cellular senescence is a stress response that imposes stable cell-cycle arrest in damaged cells, preventing their propagation in tissues. However, long-term presence of senescent cells might promote tissue degeneration and malignant transformation via secreted pro-inflammatory and matrix-remodeling factors. These factors lead to immune-cell recruitment and senescent-cell clearance. Senescent cells accumulate in tissues in advanced age. The extent of immune-system involvement in regulating age-related accumulation of senescent cells, and its consequences, are unknown. Here we show that mice with impaired cell cytotoxicity exhibit both higher senescent-cell tissue burden and chronic inflammation. They suffer from multiple age-related disorders and significantly lower survival. Strikingly, pharmacological elimination of senescent-cells by ABT-737 partially alleviates accelerated aging phenotype in these mice. In progeroid mice, impaired cell cytotoxicity further promotes senescent-cell accumulation and shortens lifespan. ABT-737 administration during the second half of life of these progeroid mice abrogates senescence signature and increases median survival. Our findings shed new light on mechanisms governing senescent-cell presence in aging, and could motivate new strategies for regenerative medicine.

2018-11-20 | GSE115401 | GEO

Transcriptomic profiling of human senescent cells in the setting of pharmacological intervention (NAD+ and NMN)

Project description:Aging and age-relataed pathologies can be delayed by specifically targeting the senescence-associated secretory phenotype (SASP), a hallmark feature of senescent cells. Achieving the goal using small molecules would have a tremendous impact on the quality of lifespan and burden of age-related chronic diseases. We report the potential of two metabolic molecules, NAD+ and NMN, to control the development of the pro-inflammatory phenotype of senescent human stromal cells. This study discloses the impact of NAD+ and NMN on the expression profile of senescent cells and provides a framework for future anti-aging administration with clear rationale.

2022-12-31 | GSE156038 | GEO

Human BATF overexpression PRO-cap

Project description:Mammalian aging is characterized by the progressive loss of tissue integrity and function manifesting in ill health and increased risk for developing multiple chronic conditions. Accumulation of senescent cells in aging tissues partly contributes to this decline as targeted depletion of senescent cells in vivo ameliorates many age-related phenotypes. However, the fundamental molecular mechanisms responsible for the decline of cellular health and fitness during senescence and aging are largely unknown. In this study, we investigated whether chromatin-mediated loss of transcriptional fidelity, known to contribute to fitness and survival in yeast and worms, also occurs during human cellular senescence and mouse aging. Our findings reveal that aberrant transcription initiation inside genes is widespread in senescence and aging. It co-occurs with changes in the chromatin landscape and formation of non-canonical transcription start sites. Interventions that alter spurious transcripts have dramatic consequences on cellular health primarily affecting intracellular signal transduction pathways. We propose that spurious transcription is a conserved hallmark of aging that promotes a noisy transcriptome and a degradation of coherent transcriptional networks.

2023-01-02 | GSE158392 | GEO

Human senescence ATAC-seq [I]

2023-01-02 | GSE156910 | GEO