Unirradiated vs. irradiated wounded planarians
Ontology highlight
ABSTRACT:
ORGANISM(S): Schmidtea mediterranea
SUBMITTER: Danielle Wenemoser
PROVIDER: E-GEOD-36945 | biostudies-arrayexpress |
REPOSITORIES: biostudies-arrayexpress
Similar Datasets
Project description:Arctic charr thrive at high densities and can live in freshwater year round, making this species especially suitable for inland, closed containment aquaculture. However, it is a cold water salmonid, which both limits where the species can be farmed and places wild populations at particular risk to climate change. Previously, we identified genes associated with tolerance and intolerance to acute, lethal temperature stress in Arctic charr. However, there remained a need to examine the genes involved in the stress response to more realistic temperatures that could be experienced during a summer heat wave in grow-out tanks that are not artificially cooled, or under natural conditions. Here, we exposed Arctic charr to moderate heat stress of 15–18ºC for 72 hours, and gill tissues extracted before, during (i.e., at 72 hrs), immediately after cooling and after 72 hours of recovery at ambient temperature (6ºC) were used for gene expression profiling by microarray and qPCR analyses. The results revealed an expected pattern for heat shock protein (Hsp) expression, which was highest during heat exposure, with significantly reduced expression (approaching control levels) quickly thereafter. We also found that the expression of numerous ribosomal proteins was significantly elevated immediately and 72 hrs after cooling, suggesting that the gill tissues were undergoing ribosomal biogenesis while recovering from damage caused by heat stress. We suggest that these are candidate gene targets for the future development of genetic markers for broodstock development or for monitoring temperature stress and recovery in wild or cultured conditions. 24 microarray slides representing 6 individuals from 4 treatment groups (Control, During, After and Recovery). One test cDNA labeled with Cy5 and the common reference aRNA labeled with Cy3 was hybridized to each slide. Reference design: 6x control fish, 6x group D fish, 6x group A fish, 6x group R fish.
2011-07-05 | E-GEOD-29610 | biostudies-arrayexpress
Project description:A M. tuberculosis transposon library was used to infect WT and iNOS-/- mice. Surviving mutants were recovered from spleens, genomic DNA was extracted, and labeled probes were synthesized from transposon ends. Probes from each WT mouse were hybridized with probes from a similar iNOS-/- mouse. Two-condition experiment, Growth in WT vs. iNOS-/- mice. Biological replicates: TraSH probe made from 5 wild type and 5 iNOS-/- mice after 3 weeks of infection and from 8 wild type and 8 iNOS-/- mice after 4 weeks of infection. Technical replicates: TraSH probe was synthesized twice from each mouse and dyes were swapped. One array contains probe from one iNOS-/- and one WT mouse. Each biological replicate has two arrays, representing technical replicate dye swaps from one iNOS-/- and one WT mouse.
2009-08-20 | E-GEOD-17706 | biostudies-arrayexpress
Project description:Bacteria can use host hormones as environment cue to modulate their pathogenic processes, which was discovered to play essential role in disease development. Actinobacillus pleuropneumoniae is one of the most important porcine respiratory pathogens causing great economic losses in the pig industry worldwide. Stress factors were found to contribute to the outcome of A. pleuropneumoniae infection. To test whether A. pleuropneumoniae could respond to host stress hormone catecholamines, the gene expression profiles after epinephrine (Epi) and norepinephrine (NE) treatment were compared with the untreated bacteria using microarray. Although the bacterial growth was not affected in the conditions tested, 157 and 104 genes associated with various function categories including many virulence factors were differentially expressed by Epi and NE treatment. 18 common genes were regulated by the two hormones, these genes included genes encoding virulence factors and potential responsors of Epi and NE. Further investigations on virulence traits demonstrated that cytotoxic activity was enhanced by Epi but repressed by NE in accordance with the regulations on apxIA. Biofilm formation was not affected by the two hormones despite that the biofilm formation gene pgaB was affected. Adhesion to host cells was induced by NE but not by Epi, possibly involving other putative adhesins affected by the hormones in addition to the autotransporter adhesin (APL_0443). Our study demonstrated that A. pleuropneumoniae could actively respond to catecholamines to control its virulence traits. The different regulated genes and effects caused by Epi and NE suggested A. pleuropneumoniae may have multiple responsive systems to sense different type of catecholamine hormones. Transcriptional profiles were analyzed using microarray to compared the epinephrine (Epi) or norepinephrine(NE) treated and untreated A. pleuropneumoniae. All samples were harvested from middle exponential phase (4 hours after sub-culture) at the OD600=1.435M-BM-10.065 for control, OD600=1.461M-BM-10.019 for Epi treated strain and OD600=1.545M-BM-10.115 for NE treated strain. Three biological replicates were conducted for each treatment. The total RNA were extracted and hybridized with the whole genome microarray of A. pleuropneumoniae. The signal intensities were normalized and transformed into log2 values. The genes with fold change M-bM-^IM-% 1.5 and P < 0.05 were selected as differentially expressed.
2012-03-19 | E-GEOD-25516 | biostudies-arrayexpress
Project description:Despite the identification of numerous autism susceptibility genes, the pathobiology of autism remains unknown. The present âcase-controlâ study takes a global approach to understanding the molecular basis of autism spectrum disorders based upon large-scale gene expression profiling. DNA microarray analyses were conducted on lymphoblastoid cell lines from over 20 sib pairs in which one sibling had a diagnosis of autism and the other was not affected in order to identify biochemical and signaling pathways which are differentially regulated in cells from autistic and nonautistic siblings. Bioinformatics and gene ontological analyses of the data implicate genes which are involved in nervous system development, inflammation, and cytoskeletal organization, in addition to genes which may be relevant to gastrointestinal or other physiological symptoms often associated with autism. Moreover, the data further suggests that these processes may be modulated by cholesterol/steroid metabolism, especially at the level of androgenic hormones. Elevation of male hormones, in turn, has been suggested as a possible factor influencing susceptibility to autism, which affects ~4 times as many males as females. Metabolic profiling of steroid hormones in lymphoblastoid cell lines from several pairs of siblings reveals higher levels of testosterone in the autistic sibling, which is consistent with the increased expression of two genes involved in the steroidogenesis pathway. Global gene expression profiling of cultured cells from ASD probands thus serves as a window to underlying metabolic and signaling deficits that may be relevant to the pathobiology of autism. Gene expression profiling of LCL from autistic (21) and nonautistic (17) siblings (4 sets of autistic twins included) were obtained using a custom-printed DNA microarray containing 39,936 elements (TIGR 40K Human array, GPL3427) and a reference design in which each sample was compared to the Stratagene Universal Human RNA standard. Following data normalization, the ratios of expression values for the autistic proband relative to his normal unaffected sibling were determined. Related siblings are identified by their common family ID# (AU****) as provided by the Autism Resource Genetic Exchange (AGRE) repository (and listed in Sample title). Differentially expressed genes were determined across all ratioed expression values for sib pairs (autistic vs. control) using one-class SAM (Statistical Analysis of Microarrays) analysis.
2010-05-15 | E-GEOD-15451 | biostudies-arrayexpress
Project description:The innate immune system responds to unique molecular signatures that are widely conserved among microbes but that are not normally present in host cells. Compounds that stimulate innate immune pathways may be valuable in the design of novel adjuvants, vaccines, and other immunotherapeutics.The cyclic dinucleotide cyclic-di-guanosine monophosphate (c-di-GMP) is a recently appreciated second messenger that plays critical regulatory roles in many species of bacteria but is not produced by eukaryotic cells. In vivo and in vitro studies have previously suggested that c-di-GMP is a potent immunostimulatory compound recognized by mouse and human cells. Here we provide evidence that c-di-GMP is sensed in the cytosol of mammalian cells via a novel immunosurveillance pathway. The potency of cytosolic signaling induced by cyclic-di- GMP is comparable to that induced by cytosolic delivery of DNA, and both nucleic acids induce a similar transcriptional profile, including triggering of type I interferons and coregulated genes via induction of TBK1, IRF3, NF-!B and MAP kinases. However, the cytosolic pathway that senses c-di-GMP appears to be distinct from all known nucleic acid-sensing pathways.Our results suggest a novel mechanism by which host cells can induce an inflammatory response to a widely produced bacterial ligand. Three-condition experiment: macrophages transfected with mono-GMP (negative control), double-stranded DNA (positive control), or cyclic-di-GMP (experimental condition). Biological replicates: two, independently treated, harvested, and hybridized to arrays. One replicate per array, except two technical replicates were performed for one of the positive control samples.
2009-07-21 | E-GEOD-16943 | biostudies-arrayexpress
Project description:Background: Osteosarcoma (OS) is a very aggressive bone tumor characterized by highly abnormal complex karyotypes. With the improved resolution offered by array comparative genomic hybridization (array CGH) platforms, it is possible to readily detect cryptic microaberrations in genomic DNA. The identification of these microaberrations in genetic syndromes is currently the focus of many array CGH studies, but there have been no analyses to date documenting the occurrence of microaberrations in tumors. Results: In this study we utilized high-resolution oligonucleotide array CGH to identify novel microaberrations under ~750 kb in four OS-derived cell lines: U-2 OS, HOS, MG-63 and SAOS-2. Comparative analysis of these alterations showed that SAOS-2 harbored the most microaberrations at 17, followed by MG-63 with 11, HOS with 9 and U-2 OS with 6. SAOS-2, which has a TP53 mutation, exhibited the highest level of chromosomal instability in previous studies by our group; whereas U-2 OS, which has wild-type p53 status, exhibited the least instability. A consensus region of gain at 5p15.33 was detected in three of the four OS-derived cell lines (HOS, MG-63 and SAOS-2) by aCGH. Of these consensus gains, one was a microaberration of 500 kb in SAOS-2, and confirmed by fluorescence in situ hybridization analysis. It should be noted that this microaberration is immediately telomeric to the TERT gene, which also showed gain. TERT is correlated with increased tumor aggression, as well as decreased progression free survival in OS patients. Experiment Overall Design: This genome-wide analysis is the first study to utilize oligonucleotide array CGH to identify microaberrations in OS, likely to contain genes involved in OS tumor oncogenesis. A better understanding of the underlying molecular genetic events leading to tumor initiation and progression could result in the identification of prognostic markers and therapeutic targets.
2008-06-18 | E-GEOD-7077 | biostudies-arrayexpress
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2010-05-14 | E-GEOD-19879 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39930 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39929 | biostudies-arrayexpress
Project description:Liver carcinogenesis induced by DEN closely mimics the pathologies observed during human liver tumor initiation and progression. DEN treatment triggered c-Jun expression lasting up to at least 1 week in mouse livers as measured by Western blots and immunohistochemical staining. DEN-induced liver tumorigenesis was also dramatically reduced in Alfp-cre+/c-jun f/f mice, in which c-Jun is constitutively deleted in hepatocytes around birth. These data unambiguously demonstrate that c-Jun is specifically required during liver cancer initiation. We searched for cell death effectors downstream of c-Jun operating in cancer initiation. Expression profiling revealed that several cell death-associated genes were deregulated by comparing Alfp-cre+/c-junf/f and Alfp-cre-/c-jun f/f livers. Mouse livers were collected before and 48hours after diethylnitrosamine treament (100mg/kg body weight). Whole genome expression profiles were analyzed using total RNAs extracted from the whole liver samples. By comparison of the gene expression profiles of these samples, genes with significantly altered expression levels will be selected and further characterized for their roles in DEN-induce liver cell death in tumor initiation.
2012-08-07 | E-GEOD-39931 | biostudies-arrayexpress