Abstract: Drought is the primary cause of global agricultural losses and represents a major threat to worldwide food security. Currently, plant biotechnology stands out as the most promising strategy to increase crop growth in rain-fed conditions. The main mechanisms underlying drought resistance have been uncovered by studies of plant physiology and by engineering crops with drought-resistant genes. However, plants with enhanced drought resistance usually display lower levels of growth, highlighting the need to search for novel strategies capable of uncoupling drought resistance from growth. Here, we show that the brassinosteroid family of receptors, in addition to promoting growth, guides phenotypic adaptation to a great variety of drought stress traits analyzed herein. Whilst mutations in the ubiquitously localized BRI1 receptor pathway show an enhanced drought resistance at the expense of plant growth, we found that vascular-enriched BRL3 receptors confer drought tolerance without penalizing overall growth. Systematic analyses reveal that upon drought stress the BRL3 receptor pathway triggers the synthesis and mobilization of osmoprotectant metabolites, mainly proline and sugars. This preferentially occurs in the vascular tissues of the roots and favors overall plant growth. Altogether, our results uncover a new role for the spatial control of BR signaling in drought tolerance, and offer a novel strategy to address food security issues in an increasingly water-limited climate. Overall design: 28 days old root system were collected from soil, quickly washed in water and flash-frozen. Experiment with a bifactorial design. Factor one is the genotype, which include WT (Col-0) and 35S:BRL3. Factor two is the condition, which include control (Properly watered) and 5 days of drought (water-hold) conditions. 3 Biological replicates were collected per each genotype and condition.
Overexpression of the vascular brassinosteroid receptor BRL3 confers drought resistance without penalizing plant growth.
Specimen part, Subject
View SamplesTranscriptome of murine testis from wild type mice and mice lacking telomerase for three generations (G3-Terc), Ku86 or both telomerase and Ku86.
Effectors of mammalian telomere dysfunction: a comparative transcriptome analysis using mouse models.
No sample metadata fields
View SamplesWhe embryonic stem cells are in vitro expanded threir telomereres lengthen, in the absence of genetic manipulations, concomitant with the loss of heterochromatic marks. In order to analyze whether there would be changes in gene expression during in vitro expansion we performed RNA-seq and found no substantial differences in gene expression at passage 6 or 16. Overall design: Embryonic stem (ES) cells were derived from blastocysts expressing GFP in the Rosa26 locus. Four independent lines of ES were in vitro expanded to passage 16. Total RNA was extracted from each independent clones, RNA was extracted and prepared for RNA-seq.
Generation of mice with longer and better preserved telomeres in the absence of genetic manipulations.
Specimen part, Cell line, Treatment, Subject
View SamplesRecent studies suggest that telomerase promotes cell growth by mechanisms that extend beyond the rescue of critically short telomeres. The in vitro model of mTert overexpressing MEFs recapitulates fundamental aspects of the growth-promoting effects of mTert in vivo. First, in Terc-proficient cells, mTert overexpression favors escape from replicative senescence and enhances anchorage-independent growth in response to oncogenic stress, which fits well with previous data showing that mTert overexpression promotes tumor formation. Second, in Terc-deficient cells, retroviral transduction with mTert results in a delayed onset of immortalization and impairs colony formation in response to oncogenic stress, which is in agreement with the inhibitory effect of mTert overexpression on tumorigenesis in a Terc null mouse background. To unravel the molecular targets of telomerase that impact on cell growth, we compared the transcriptome of MEFs, before and after mTert introduction. We found that ectopic expression of mTert was associated with detectable gene expression changes (greater than 1.5-fold; validated by qRT-PCR) of 26 transcripts. Analysis of the observed transcriptional changes indicates that ectopic expression of mTert suppresses in a coordinated manner functionally related genes with overlapping roles in growth arrest, resistance to transformation, and apoptosis. We show that the majority of the telomerase target genes are growth-inhibitory, transforming growth factor-beta (TGF-beta) -inducible genes and provide functional evidence for the potential of telomerase to abrogate TGF-beta -mediated growth inhibition. Thus, in line with the current view that the diversity of TGF-beta responses is not so much a consequence of the use of different signaling pathways but caused by different ways of reading the output from the same basic pathway, we propose that the telomerase status of a cell creates a gene expression pattern that determines how cells read growth inhibitory signals, among them signals propagated through the TGF-beta pathway.
Expression of mTert in primary murine cells links the growth-promoting effects of telomerase to transforming growth factor-beta signaling.
No sample metadata fields
View SamplesWe profiled total mRNA of pancreas and kidney tissues of 3 different strains (p53-null; In4a/Arf-null and WT) of reprogrammable mouse lines (they all express OCT4, SOX2, KLF4, C-MYC under the control of a tetracycline promoter, activated by doxycycline) Overall design: 5 mice of each genotype were treated with doxycycline to induce the expression of the reprogramming factors, they were sacrificed and total mRNA was extracted from pancreas and kidney tissues (we mapped >24M reads per sample)
Tissue damage and senescence provide critical signals for cellular reprogramming in vivo.
Specimen part, Cell line, Subject
View SamplesBrucella suis infects macrophages and dendritic cells. Wild boars act as reservoirs and carriers of Brucella suis biovar 2, and there is evidence that wild boar can be the main source of infection for domestic pigs through the venereal route. Transmission through this route could be an important path for disesease dissemination. The result from this study will contribute to the overall understanding of the molecular pathogenic mechanisms involved during Brucella suis infection in European wild boar.
Gene expression changes in spleens of the wildlife reservoir species, Eurasian wild boar (Sus scrofa), naturally infected with Brucella suis biovar 2.
Specimen part, Disease
View SamplesThis SuperSeries is composed of the SubSeries listed below.
Isolation and in vitro expansion of human colonic stem cells.
Sex, Specimen part, Subject
View SamplesUsing the surface marker EPHB2, we have FACS-purified and profiled stem cell-enriched cell fractions from normal human mucosa, crypt proliferative progenitors and late transient amplifying cells to define a gene expression program specific for normal human colon epithelial stem cells
Isolation and in vitro expansion of human colonic stem cells.
Specimen part, Subject
View SamplesGene expression from bone-marrow drived macrophages of WT and SREBP-1a deficient mice
Linking lipid metabolism to the innate immune response in macrophages through sterol regulatory element binding protein-1a.
No sample metadata fields
View SamplesCarcinoma development in colorectal cancer (CRC) is driven by genetic alterations in numerous signaling pathways. Alterations in the RAS-ERK1/2 pathway are associated with the shortest overall survival for patients after diagnosis of CRC metastatic disease, but how RAS-ERK signaling regulates CRC metastasis is still unknown.
ERK1/2 Signaling Induces Upregulation of ANGPT2 and CXCR4 to Mediate Liver Metastasis in Colon Cancer.
Cell line, Treatment
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