We show that infant trauma, as modeled by infant paired odor-shock conditioning, results in later life depressive-like behavior that can be modulated by learned infant cues (i.e., odor previously paired with shock). We have previously shown that this infant attachment odor learning paradigm results in the creation of a new artificial maternal odor that is able to control pup behavior and retain its value throughout development. Here, we assess the mechanism by which this artificial maternal odor is able to rescue depressive-like behavior and show that this anti-depressant like effect results in glucocorticoid and serotonin (5-HT) related changes in amygdala gene expression and is dependent on amygdala 5-HT. Furthermore, increasing amygdala 5-HT and blocking corticosterone (CORT) in the absence of odor mimics the adult rescue effects elicited by the artificial maternal odor, suggesting a mechanism by which odor presentation exerts its repair effects.
Enduring good memories of infant trauma: rescue of adult neurobehavioral deficits via amygdala serotonin and corticosterone interaction.
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 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 SamplesWe examined patterns of gene expression in two independent colonies of both M and S molecular forms of Anopheles gambiae at each of three developmental stages of interest: late larvae, sugar-fed virgin females, and gravid females. For each colony, replicates were derived from independent RNA samples extracted from different cohorts to ensure that trends were reproducible. In addition, each replicate was derived from larvae (adults) drawn from three pans (cages) to minimize the contribution of any individual pan to variation between samples. Data were obtained from a total of five biological replicates per mosquito colony.
Differential gene expression in incipient species of Anopheles gambiae.
Sex
View SampleshTERT/cdk4 immortalized myogenic human cell lines represent an important tool for skeletal muscle research, being used as therapeutically-pertinent models of various neuromuscular disorders and in numerous fundamental studies of muscle cell function. However, the cell cycle is linked to other cellular processes such as integrin regulation, the PI3K/Akt pathway, and microtubule stability, raising the question as to whether transgenic modification of the cell cycle results in secondary effects that could undermine the validity of these cell models. Here we subjected healthy and disease lines to intensive transcriptomic analysis, comparing immortalized lines with their parent primary populations in both differentiated and undifferentiated states, and testing their myogenic character by comparison with non-myogenic (CD56-negative) cells. We found that immortalization has no measurable effect on the myogenic cascade or on any other cellular processes, and that it was protective against the systems level effects of senescence that are observed at higher division counts of primary cells.
Skeletal muscle characteristics are preserved in hTERT/cdk4 human myogenic cell lines.
Specimen part, Disease, Disease stage
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.
Specimen part
View SamplesOur goal was to transcriptionally profile Prdm1+ cell lineages of maternal and embryonic origin in mid-gestation mouse placenta in order to study vascular mimicry and additional processes in the placenta. Overall design: Profiling of 61 single cells and 17 clusters of 2 or 3 cells chosen based on expression of Prdm1, a paternally inherited Prdm1-Venus fluorescent reporter, progenitor trophoblast marker Gjb3 and spiral artery trophoblast giant cell marker Prl7b1.
Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.
Specimen part, Cell line, Subject
View SamplesExpression profiling of wild-type and Prdm1 null mouse trophoblast giant cell cultures using Illumina whole genome mouse V2 arrays.
Single-cell RNA-seq reveals cell type-specific transcriptional signatures at the maternal-foetal interface during pregnancy.
Specimen part
View SamplesSmyd3 is a histone methyltransferase implicated in tumorigenesis. Here we show that Smyd3 expression in mice is required but not sufficient for chemically induced liver and colon cancer formation. In these organs Smyd3 is functioning in the nucleus as a direct transcriptional activator of several key genes involved in cell proliferation, epithelial-mesenchymal transition, JAK/Stat3 oncogenic pathways, as well as of the c-myc and b-catenin oncogenes. Smyd3 specifically interacts with H3K4Me3-modified histone tails and is recruited to the core promoter regions of many but not all active genes. Smyd3 binding density on target genes positively correlates with increased RNA Pol-II density and transcriptional outputs. The results suggest that Smyd3 is an essential transcriptional potentiator of a multitude of cancer-related genes. Overall design: Standard Smyd3-deficient (Smyd3-KO) mice were generated using gene-trap ES cell clones (AS0527 from International Gene Trap Consortium), in which a selection cassette, containing the splice acceptor site from mouse EN2 exon 2 followed by the beta-galactosidase and neomycin resistance gene fusion gene and the SV40 polyadenylation sequence was inserted into the 5th intron of the Smyd3 gene. The resulting mice were devoid of Smyd3 mRNA and protein in all tissues, including liver and colon. For the generation of Smyd3-Tg mice the open reading frame of the mouse Smyd3 cDNA, which contained 3 Flag epitopes at the 3’ end was inserted into the StuI site of the pTTR1-ExV3 plasmid (Yan et al, 1990). The 6.8 kb HindIII fragment containing the mouse transthyretin enhancer/promoter, intron 1, Smyd3 cDNA, three Flag epitopes and SV40 poly-A site was used to microinject C57Bl/6 fertilized oocytes. Founder animals were identified by Southern blotting and crossed with F1 mice to generate lines. Specific overexpression in the liver was tested by RT-PCR analysis in different tissues.
Smyd3 Is a Transcriptional Potentiator of Multiple Cancer-Promoting Genes and Required for Liver and Colon Cancer Development.
No sample metadata fields
View SamplesIn this study, we characterize transciprtional phenotypes of airway macrophagages (AMs) throughout homeostatsis, inflammation, and repair at single cell granularity. We confirm that cell origin is the major determinant of AM programing and describe two previously uncharacterized, transcriptionally distinct subdivisions of AMs based on proliferative capacity and inflammatory programing. Overall design: We stimulated mice with LPS and then sampled FACs sorted airway macrophage cells using BAL at Days 0, 3, and 6 and sequenced 1,134 cells from these three groups using RNA-seq
Single cell RNA sequencing identifies unique inflammatory airspace macrophage subsets.
Specimen part, Cell line, Subject
View Samples