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Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation

ABSTRACT: Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation

PROVIDER: PRJNA1066222 | ENA |

REPOSITORIES: ENA

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			Action	DRS
	SRR27564100_1.fastq.gz	Fastqsanger.gz
	SRR27564100_2.fastq.gz	Fastqsanger.gz
	SRR27564101_1.fastq.gz	Fastqsanger.gz
	SRR27564101_2.fastq.gz	Fastqsanger.gz
	SRR27564087_1.fastq.gz	Fastqsanger.gz

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Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Long]

Project description:The generation of new neurons from neural stem cells is tightly controlled by transcriptional programs. To induce cell fate switches that establish neuronal identities, differentiating neural precursor cells (NPCs) must undergo rapid and dynamic gene expression changes. However, the neuronal fate-determining molecular events that precede NPC differentiation are incompletely understood. Using high temporal resolution transcriptional profiling of adult hippocampal NPC differentiation, we here identified the activating transcription factors Atf3 and Atf4 as early switch regulators that drive NPC fate and control neuron formation. We found that Atf3/4 are rapidly upregulated in NPCs upon induction of differentiation and drive dynamic gene expression changes associated with neurogenesis. Pharmacological and genetic perturbation of Atf4 demonstrated its importance for neuron formation. Sustained overexpression of Atf3 hampered neurogenesis by repressing long non-coding RNA Miat. Our results demonstrate the critical role of an Atf3/Atf4-controlled transcriptional network in driving early molecular events during neurogenesis.

2024-01-18 | GSE253304 | GEO

Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Short]

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Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Long]

Project description:Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Long]

| PRJNA1065003 | ENA

Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Short]

Project description:Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation [Short]

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Activating transcription factors Atf3/4 drive early molecular events during neural stem cell differentiation and control neuron formation [RNA-seq]

2024-01-18 | GSE253374 | GEO

Activating transcription factors Atf3/Atf4 drive early molecular events preceding neural stem cell differentiation and control neuron formation

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

2024-01-18 | GSE253534 | GEO

Deciphering the direct transcriptional targets of the Drosophila Activating transcription factor 3 (Atf3) via ChIp-seq: Atf3 bridges the gap between cell polarity and the nucleus

Project description:Epithelial structure and function are governed by evolutionarily conserved signaling programs. The Drosophila Activating transcription factor 3 (Atf3) prevents epithelial cell replacement during abdominal morphogenesis, yet its transcriptional targets are unknown. Here we demonstrate that Atf3 positively and negatively regulates target genes central to cytoskeleton dynamics and adhesion. Epithelial clones overexpressing Atf3 are enriched for basolateral proteins at the expense of apical identity. Strikingly, Atf3 functions downstream of the Scrib polarity module. Depleting either scrib or dlg1 induces atf3 expression, while loss of atf3 suppresses differentiation and polarity defects in cells deficient for the Scrib complex

2018-02-20 | GSE71206 | GEO

ATF3 is a novel regulator of mouse neutrophil migration.

Project description:Expression of the activating transcription factor 3 (ATF3) gene is induced by Toll-like receptor (TLR) signaling. In turn, ATF3 protein inhibits the expression of various TLR-driven pro-inflammatory genes. Given its counter-regulatory role in diverse innate immune responses, we defined the effects of ATF3 on neutrophilic airway inflammation in mice. ATF3 deletion was associated with increased lipopolysaccharide (LPS)-driven airway epithelia production of CXCL1, but not CXCL2, findings concordant with a consensus ATF3-binding site identified solely in the Cxcl1 promoter. Unexpectedly, ATF3-deficient mice did not exhibit increased airway neutrophilia after LPS challenge. Bone marrow chimeras revealed a specific reduction in ATF3-/- neutrophil recruitment to wild type lungs. In vitro, ATF3-/- neutrophils exhibited a profound chemotaxis defect. Global gene expression analysis identified ablated Tiam2 expression in ATF3-/- neutrophils. TIAM2 regulates cellular motility by activating Rac1-mediated focal adhesion disassembly. Notably, ATF3-/- and ATF3-sufficient TIAM2 knockdown neutrophils, both lacking TIAM2, exhibited increased focal complex area, along with excessive CD11b-mediated F-actin polymerization. Together, our data describe a dichotomous role for ATF3-mediated regulation of neutrophilic responses: inhibition of neutrophil chemokine production, but promotion of neutrophil chemotaxis. Ly6G+ neutrophils were purified by magnetic beads from WT or ATF3 KO bone marrow and RNA was immediately isolated for global gene expression using microarrays.

2014-04-05 | E-GEOD-53973 | biostudies-arrayexpress

Exercise-induced angiogenesis is dependent on metabolically primed ATF3/4+ endothelial cells

Project description:Exercise is a powerful driver of physiological angiogenesis during adulthood, but the mechanisms of exercise-induced vascular expansion are poorly understood. We explored endothelial heterogeneity in skeletal muscle and identified two capillary muscle endothelial cells (mEC) populations which are characterized by differential expression of ATF3/4. Spatial mapping showed that ATF3/4 + mECs are enriched in red oxidative muscle areas while ATF3/4 low ECs lie adjacent to white glycolytic fibers. In vitro and in vivo experiments revealed that red ATF3/4 + mECs are more angiogenic when compared to white ATF3/4 low mECs. Mechanistically, ATF3/4 in mECs control genes involved in amino acid uptake and metabolism and metabolically prime red (ATF3/4 + ) mECs for angiogenesis. As a consequence, supplementation of non-essential amino acids and overexpression of ATF4 increased proliferation of white mECs. Finally, deleting Atf4 in ECs impaired exercise-induced angiogenesis. Our findings illustrate that spatial metabolic angiodiversity determines the angiogenic potential of muscle ECs.

2021-06-15 | GSE174785 | GEO

RNA-Seq experiment to identify genes regulated by ATF4

Project description:Activating Transcription Factor 4 (ATF4) is a transcription factor induced by the integrated stress response (ISR). This experiment is a genome-wide profiling of ATF4-dependent RNA expression in human HAP-1 cells. HAP-1 is a near-haploid human cell line that was derived from KBM-7 cells isolated from a patient with Chronic Myelogenous Leukemia. We analyzed WT and ATF4 KO cells. We induced ATF4 expression by mimicking amino acid starvation with the drug histidinol. RNA expression profiles were generated for WT and ATF4 KO HAP1 cells. ATF4 genes were mutated using Cas9 genome editing technology. Amino acid starvation was mimicked by treating WT and ATF4 KO cells with 2 mM histidinol for 24 hours, which increases ATF4 expression.

2015-08-28 | E-GEOD-69308 | biostudies-arrayexpress

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