The signaling pathway for Nodal, a ligand of the transforming growth factor-beta (TGF-beta) superfamily, plays a central role in regulating the maintenance and/or differentiation of stem cell types that can be derived from the peri-implantation mouse embryo. Extraembryonic endoderm stem (XEN) cells are derived from the primitive endoderm of the blastocyst, which normally gives rise to the parietal and the visceral endoderm in vivo, but XEN cells do not contribute efficiently to the visceral endoderm in chimeric embryos. We have found that treatment of XEN cells with Nodal and/or Cripto, an EGF-CFC co-receptor for Nodal, results in up-regulation of markers for visceral endoderm as well as anterior visceral endoderm (AVE). Re-introduction of treated XEN cells into chimeric embryos by blastocyst injection or morula aggregation results in contribution to visceral endoderm and AVE. In culture, XEN cells do not express Cripto, but do express the related EGF-CFC co-receptor Cryptic and require Cryptic for Nodal signaling. Notably, the response to Nodal can be blocked by treatment with the ALK4/ALK5/ALK7 inhibitor SB431542, but Cripto treatment is unaffected, suggesting that its activity is independent of type I activin receptors. Gene set enrichment analysis of genome-wide expression signatures generated from XEN cells under these treatment conditions confirms the differing responses of Nodal- and Cripto-treated XEN cells to SB431542. Our findings define distinct pathways for Nodal and Cripto in the differentiation of visceral endoderm and AVE from XEN cells, and provide new insights into the specification of these cell types in vivo.
Regulation of extra-embryonic endoderm stem cell differentiation by Nodal and Cripto signaling.
Cell line, Treatment, Time
View SamplesTissue injury, such as incisional wound, results in an inflammatory response as well as acute to chronic mechanical and thermal pain. It is now understood that there is a strong contribution of these immune cells to the pain phenotype.
CD11b+Ly6G- myeloid cells mediate mechanical inflammatory pain hypersensitivity.
Sex, Age
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Strain-specific activation of the NF-kappaB pathway by GRA15, a novel Toxoplasma gondii dense granule protein.
Specimen part
View SamplesToxoplasma strains have been shown to modulate host cell transcription. We have found a type II Toxoplasma gene, GRA15, which activates the nuclear translocation of the NF-kappaB p65 transcription factor.
Strain-specific activation of the NF-kappaB pathway by GRA15, a novel Toxoplasma gondii dense granule protein.
Specimen part
View SamplesToxoplasma strains have been shown to modulate host cell transcription. We have found a type II Toxoplasma gene, GRA15, which activates the nuclear translocation of the NF-kappaB p65 transcription factor.
Strain-specific activation of the NF-kappaB pathway by GRA15, a novel Toxoplasma gondii dense granule protein.
Specimen part
View Samplesaffy_pop_2011_08 - poplar bent study - genes regulated by PtaZFP2 in absence of mechanical stress - genes regulated by PtaZFP2 after one bending.Species: Populus tremula x Populus alba-- The laboratory previously established a poplar transgenic line overexpressing PtaZFP2 under the control of an estradiol-inducible promoter. - the experiment, conducted on 3-month-old hydroponically-grown poplars, consists in the comparison of WT poplars treated with estradiol and the PtaZFP2-overexpressing line treated with estradiol. We also compared unbent and bent PtaZFP2-overexpressing poplars. The applied strain is quantitatively controlled (Coutand & Moulia, 2000, JExpBot; coutand et al., 2009, Plant Physiology) -
The zinc finger protein PtaZFP2 negatively controls stem growth and gene expression responsiveness to external mechanical loads in poplar.
Treatment
View SamplesThe Toxoplasma type I ROP16 kinase directly activates the host STAT3 and STAT6 transcription factors and regulates the expression of many host genes. However, many of genes lack known STAT3/6 transcription factor binding sites in their promoter regions.
Toxoplasma gondii rhoptry 16 kinase promotes host resistance to oral infection and intestinal inflammation only in the context of the dense granule protein GRA15.
Specimen part
View Samplesaffy_pop_2011_08 - poplar estradiol study - genes regulated by PtaZFP2 in absence of mechanical stress - genes regulated by PtaZFP2 after one bending.Species: Populus tremula x Populus alba-The laboratory previously established a poplar transgenic line overexpressing PtaZFP2 under the control of an estradiol-inducible promoter. - the experiment, conducted on 3-month-old hydroponically-grown poplars, consists in the comparison of WT poplars treated with estradiol and the PtaZFP2-overexpressing line treated with estradiol. We also compared unbent and bent PtaZFP2-overexpressing poplars. The applied strain is quantitatively controlled (Coutand & Moulia, 2000, JExpBot; coutand et al., 2009, Plant Physiology)
The zinc finger protein PtaZFP2 negatively controls stem growth and gene expression responsiveness to external mechanical loads in poplar.
Treatment
View SamplesThe Toxoplasma type I ROP16 kinase directly activates the host STAT3 and STAT6 transcription factors and when transgenically expressed in the orally virulent type II strain, promotes host resistance to oral challenge.
Toxoplasma gondii rhoptry 16 kinase promotes host resistance to oral infection and intestinal inflammation only in the context of the dense granule protein GRA15.
Specimen part
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Genetic basis for phenotypic differences between different Toxoplasma gondii type I strains.
Specimen part, Treatment
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