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accession-icon GSE47778
DAF-16/FoxO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage
  • organism-icon Caenorhabditis elegans
  • sample-icon 51 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

This SuperSeries is composed of the SubSeries listed below.

Publication Title

DAF-16/FOXO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage.

Sample Metadata Fields

Treatment

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accession-icon GSE51162
DAF-16/FoxO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage [N2, daf-2, daf-16, daf-2;daf-16]
  • organism-icon Caenorhabditis elegans
  • sample-icon 36 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists.

Publication Title

DAF-16/FOXO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage.

Sample Metadata Fields

Treatment

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accession-icon GSE51161
DAF-16/FoxO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage [N2, xpa-1]
  • organism-icon Caenorhabditis elegans
  • sample-icon 15 Downloadable Samples
  • Technology Badge Icon Affymetrix C. elegans Genome Array (celegans)

Description

Genome maintenance defects cause complex disease phenotypes characterized by developmental failure, cancer susceptibility and premature aging. It remains poorly understood how DNA damage responses function during organismal development and maintain tissue functionality when DNA damage accumulates with aging. Here we show that the FoxO transcription factor DAF-16 is activated in response to DNA damage during development while the DNA damage responsiveness of DAF-16 declines with aging. We find that in contrast to its established role in mediating starvation arrest, DAF-16 alleviates DNA damage induced developmental arrest and even in the absence of DNA repair promotes developmental growth and enhances somatic tissue functionality. We demonstrate that the GATA transcription factor EGL-27 co-regulates DAF-16 target genes in response to DNA damage and together with DAF-16 promotes developmental growth. We propose that EGL-27/GATA activity specifies DAF-16 mediated DNA damage responses to enable developmental progression and to prolong tissue functioning when DNA damage persists.

Publication Title

DAF-16/FOXO and EGL-27/GATA promote developmental growth in response to persistent somatic DNA damage.

Sample Metadata Fields

Treatment

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accession-icon SRP120583
PTCD1 is required for 16S rRNA maturation complex stability and mitochondrial ribosome assembly
  • organism-icon Mus musculus
  • sample-icon 48 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Differential gene expression as a consequence of PTCD1 loss Overall design: We used RNA from control and PTCD1 knockout mice to investigate changes at the RNA level in response to PTCD1 loss

Publication Title

PTCD1 Is Required for 16S rRNA Maturation Complex Stability and Mitochondrial Ribosome Assembly.

Sample Metadata Fields

Specimen part, Subject

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accession-icon SRP054257
PATZ1 is a DNA damage responsive transcription factor that inhibits p53 function
  • organism-icon Mus musculus
  • sample-icon 6 Downloadable Samples
  • Technology Badge IconIllumina HiSeq 2000

Description

Insults to cellular health cause p53 protein accumulation and loss of p53 function leads to tumorigenesis. Thus, p53 has to be tightly controlled. Here we report that the BTB/POZ domain transcription factor PATZ1 (MAZR), previously known for its transcriptional suppressor functions in T lymphocytes, is a crucial regulator of p53. The novel inhibitory role of PATZ1 on the p53 protein marks it as a proto-oncogene. PATZ1 deficient cells have reduced proliferative capacity which we assess by RNASeq and real time cell growth rate analysis. PATZ1 modifies the expression of p53 target genes associated with cell proliferation gene ontology terms. Moreover, PATZ1 regulates several genes involved in cellular adhesion and morphogenesis. Significantly, treatment with the DNA damage inducing drug doxorubicin results in the loss of the PATZ1 transcription factor, as p53 accumulates. We find that PATZ1 binds to p53 and inhibits p53 dependent transcription activation. We examine the mechanism of this functional inhibitory interaction and demonstrate that PATZ1 excludes p53 from DNA binding. This study documents PATZ1 as a novel player in the p53 pathway. Overall design: RNA-seq was used to define differentially expressed genes in wild-type and PATZ1-/- MEFs. Each sample was represented in triplicate.

Publication Title

PATZ1 Is a DNA Damage-Responsive Transcription Factor That Inhibits p53 Function.

Sample Metadata Fields

No sample metadata fields

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accession-icon SRP178252
Gastric Lgr5+ cells are programmed by Rspo3 to shield the gland from infection
  • organism-icon Mus musculus
  • sample-icon 2 Downloadable Samples
  • Technology Badge IconNextSeq 500

Description

R-spondin (Rspo) signaling is crucial for stem cell renewal and tissue homeostasis in the gastrointestinal tract. In the stomach, Rspo is secreted from myofibroblasts and controls epithelial gland regeneration by inducing proliferation of Wnt-responsive Axin2+ cells in the isthmus of the gland. Infection with H. pylori results in increased expression of stromal Rspo, leading to an expansion of Axin2+ isthmus stem cells and gland hyperplasia. Lgr5+ cells in the gland base are exposed to Rspo3 but the effects of this are not well understood. Here we demonstrate that apart from its activity as a mitogen, endogenous Rspo3 regulates gene expression of Lgr5+ cells in the gastric gland base. Surprisingly, Rspo3 induces differentiation within the Lgr5+ compartment towards secretory deep mucous cells. Moreover, the Rspo3-Lgr5 axis turns out to be a stimulus of epithelial antimicrobial defense. Infection with H. pylori induces a strong antimicrobial response, with Lgr5+ cells expressing antimicrobial compounds that are secreted into the lumen in an Rspo3-dependent manner. Depletion of Lgr5+ cells or knockout of Rspo3 in myofibroblasts leads to hyper-colonization of gastric glands, including the stem cell compartment, whereas systemic application of recombinant Rspo clears H. pylori from the glands. We provide an intriguing, unexpected feature of the Rspo3-Lgr5 axis in the stomach, exhibiting antimicrobial self-protection of the gland to protect the stem cell compartment from invading pathogens. Overall design: Lgr5eGFP reporter mice were infected with H. pylori for 2 months, uninfected mice served as controls. Mice were sacrificed and isolated, sorted Lgr5eGFP+ cells from the stomach antrum were used for single cell RNAseq using the 10x genome platform.

Publication Title

R-spondin-3 induces secretory, antimicrobial Lgr5<sup>+</sup> cells in the stomach.

Sample Metadata Fields

Specimen part, Cell line, Subject

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Cite refine.bio

Casey S. Greene, Dongbo Hu, Richard W. W. Jones, Stephanie Liu, David S. Mejia, Rob Patro, Stephen R. Piccolo, Ariel Rodriguez Romero, Hirak Sarkar, Candace L. Savonen, Jaclyn N. Taroni, William E. Vauclain, Deepashree Venkatesh Prasad, Kurt G. Wheeler. refine.bio: a resource of uniformly processed publicly available gene expression datasets.
URL: https://www.refine.bio

Note that the contributor list is in alphabetical order as we prepare a manuscript for submission.

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