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MOF maintains Transcriptional Programs required to protect cells against Stress

ABSTRACT: This SuperSeries is composed of the SubSeries listed below.

OTHER RELATED OMICS DATASETS IN: PRJNA289591PRJNA265050PRJNA289727

ORGANISM(S): Mus musculus

PROVIDER: GSE70707 | GEO | 2015/07/13

SECONDARY ACCESSION(S): PRJNA289591

REPOSITORIES: GEO

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MOF maintains transcriptional programs regulating cellular stress response.

Project description:MOF (MYST1, KAT8) is the major H4K16 lysine acetyltransferase (KAT) in Drosophila and mammals and is essential for embryonic development. However, little is known regarding the role of MOF in specific cell lineages. Here we analyze the differential role of MOF in proliferating and terminally differentiated tissues at steady state and under stress conditions. In proliferating cells, MOF directly binds and maintains the expression of genes required for cell cycle progression. In contrast, MOF is dispensable for terminally differentiated, postmitotic glomerular podocytes under physiological conditions. However, in response to injury, MOF is absolutely critical for podocyte maintenance in vivo. Consistently, we detect defective nuclear, endoplasmic reticulum and Golgi structures, as well as presence of multivesicular bodies in vivo in podocytes lacking Mof following injury. Undertaking genome-wide expression analysis of podocytes, we uncover several MOF-regulated pathways required for stress response. We find that MOF, along with the members of the non-specific lethal but not the male-specific lethal complex, directly binds to genes encoding the lysosome, endocytosis and vacuole pathways, which are known regulators of podocyte maintenance. Thus, our work identifies MOF as a key regulator of cellular stress response in glomerular podocytes.

| S-EPMC4893634 | biostudies-literature

Genome-wide analysis of p53 transcriptional programs in B cells upon exposure to genotoxic stress in vivo

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2015-08-24 | E-GEOD-71180 | biostudies-arrayexpress

SMAD4 maintains the Fluid Shear Stress set point to protect against Arterial-Venous Malformations

Project description:Vascular networks form, remodel and mature under the influence of both fluid shear stress (FSS) and soluble factors. Physiological FSS promotes and maintains vascular stability via synergy with Bone Morphogenic Protein 9 (BMP9) and BMP10. Conversely, mutation of the BMP receptors ALK1, Endoglin or the downstream effector SMAD4 leads to Hereditary Hemorrhagic Telangiectasia (HHT), characterized by fragile and leaky arterial-venous malformations (AVMs). But how endothelial cells (EC) integrate FSS and BMP signals in vascular development and homeostasis, and how mutations give rise to vascular malformations is not well understood. Here, we aimed to elucidate the mechanism of synergy between fluid shear stress and SMAD signaling in vascular stability and its failure in HHT. We have now found that loss of Smad4 increases ECs’ sensitivity to flow by lowering the FSS set point with resulting AVMs exhibiting features of excessive flow-mediated morphological responses. Mechanistically, loss of Smad4 disinhibits flow-mediated Klf4-Tie2-PI3K/Akt signaling leading to increased EC proliferation and loss of arterial identity due to Klf4-mediated repression of cyclin dependent Kinase (CDK) inhibitors, CDKN2A and CDKN2B. Thus, AVMs caused by Smad4 deletion are characterized by chronic high flow remodeling with excessive EC proliferation and loss of arterial identity as triggering events.

2023-07-03 | GSE232443 | GEO

The Tif1Beta-Hp1 system maintains transcriptional integrity of hematopoietic stem cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-11-06 | E-GEOD-48987 | biostudies-arrayexpress

Activation of RXRα reprograms chromatin accessibility to protect against acute kidney injury.

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

2022-11-05 | GSE197815 | GEO

A threshold of endogenous stress is required to engage cellular response to protect against mutagenesis.

Project description:Endogenous stress represents a major source of genome instability, but is in essence difficult to apprehend. Incorporation of labeled radionuclides into DNA constitutes a tractable model to analyze cellular responses to endogenous attacks. Here we show that incorporation of [(3)H]thymidine into CHO cells generates oxidative-induced mutagenesis, but, with a peak at low doses. Proteomic analysis showed that the cellular response differs between low and high levels of endogenous stress. In particular, these results confirmed the involvement of proteins implicated in redox homeostasis and DNA damage signaling pathways. Induced-mutagenesis was abolished by the anti-oxidant N-acetyl cysteine and plateaued, at high doses, upon exposure to L-buthionine sulfoximine, which represses cellular detoxification. The [(3)H]thymidine-induced mutation spectrum revealed mostly base substitutions, exhibiting a signature specific for low doses (GC?>?CG and AT?>?CG). Consistently, the enzymatic activity of the base excision repair protein APE-1 is induced at only medium or high doses. Collectively, the data reveal that a threshold of endogenous stress must be reached to trigger cellular detoxification and DNA repair programs; below this threshold, the consequences of endogenous stress escape cellular surveillance, leading to high levels of mutagenesis. Therefore, low doses of endogenous local stress can jeopardize genome integrity more efficiently than higher doses.

| S-EPMC4942696 | biostudies-literature

H3K36 methylation maintains cell identity by regulating opposing lineage programs

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

2023-02-21 | GSE203492 | GEO

SIRT6 is required for the integrated stress response and resistance to transcriptional inhibition

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

2023-03-15 | GSE181606 | GEO

Distinct transcriptional programs controlled by ERG and ETV1 in prostate cells

Project description:This SuperSeries is composed of the SubSeries listed below. Refer to individual Series

2013-03-01 | E-GEOD-39388 | biostudies-arrayexpress

MOF acetylates Lamin A/C to protect against chromothripsis

Project description:MOF-mediated acetylation of Lamin A/C is essential for the maintenance of nuclear architecture and genomic stability in mammalian cells.

| PRJEB27801 | ENA

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