Skin microbiome of Alytes obstetricans tadpoles
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ABSTRACT:
PROVIDER: PRJEB48029 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:Alytes obstetricians skin bacterial microbiome Raw sequence reads
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Project description:Skin microbiome composition of tadpoles of three different amphibian species (Alytes obstetricans, Rana temporaria, Bufo bufo)
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Project description:Skin microbiome composition of tadpoles of three different amphibian species (Alytes obstetricans, Rana temporaria, Bufo bufo)
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Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. The tadpoles revert to a normal phenotype upon removal of the larval salamander threat. The objective of the present study was to use our own fabricated tadpole Rana pirica cDNA microarray to profile gene expression patterns during the predation threat. Experimental design used to produce control, bulgy morph and reversion type tadpoles for the microarray analysis was as follows. One group of tadpoles was placed with a larval salamander for 4 days to induce formation of the bulgy morph phenotype; the predator was then removed and the tadpoles were allowed to revert to the normal phenotype for 4 days. This group is termed “8 day out tadpoles”. A second group of tadpoles was placed with the predator for the full 8 days. The control group was not exposed to a predator. Tadpoles from the predator induced groups were sampled at 6 hours, 4 days and 8 days, those from the control group at 0 hour, 4 days, and 8 days. The comparative design of the microarray analysis was performed as (Exp 6 hours VS Cont 0 hours), (Exp 4 days VS Cont 4 days), (Exp 8 days VS Cont 8 days), and (Exp 8 days-Out VS Exp 8 days), respectively. These analyses were performed in triplicate with a dye swap experiment. Samples 0hr~8days were as follows. Sample plate (1~3A):Channel 1-Cy5 Experiment,Channel 2-Cy3 Control. Sample plate (1~3B):Channel 1-Cy5 Control, Channel 2-Cy3 Experiment. In case of 8day-out samples were as follows. Sample plate (1~3A):Channel 1-Cy5 8day-out,Channel 2-Cy3 full 8day. Sample plate (1~3B):Channel 1-Cy5 full 8day,Channel 2-Cy3 8day-out.
2009-06-15 | E-GEOD-12005 | biostudies-arrayexpress
Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. The tadpoles revert to a normal phenotype upon removal of the larval salamander threat. The objective of the present study was to use our own fabricated tadpole Rana pirica cDNA microarray to profile gene expression patterns during the predation threat.
2009-06-15 | GSE12005 | GEO
Project description:DNA damage can promote altered RNA splicing and decreased gene expression (Gregersen and Svejstrup, 2018; Milek et al., 2017; Munoz et al., 2009; Shkreta and Chabot, 2015), and aberrant splicing is implicated in neurodegenerative diseases including amyotrophic lateral sclerosis (ALS), Fragile X syndrome and spinal muscular atrophy (SMA) (Conlon et al., 2016; Jia et al., 2012; Loomis et al., 2014; Qiu et al., 2014; Scotti and Swanson, 2016). Therefore, we used RNA-seq data to assess RNA-splicing in double-mutant brain tissue using multivariate analysis of transcriptional splicing (rMATS) (Shen et al., 2014) and a splicing deficiency score algorithm (Bai et al., 2013) to assess intron retention.
2021-12-14 | GSE174841 | GEO
Project description:Chytrid fungal (Bd)/Ranavirus Co-infection Model using Alytes muletensis frogs: Evaluation of Host/Pathogen Interactions using the C-bellyskin Organ Culture Method
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Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. Whereas, dragon fly also induced higher tail tadpole. The tadpoles revert to a normal phenotype upon removal of the larval salamander or dragon fly threat. The objective of the present study was to use Affymetrix Xenopus Genechip to profile gene expression in the tail tissue by different predation threat. Tadpoles of Rana pirica treated with larvae salamander for 8days (S1, S2, S3) or dragon fly for 8days (Y1,Y2, Y3) were analyzed with triplicate. Removal experiments were also treated with predators for 4days and then removed predators from tadpoles (-S1,-S2, -S3) or (-Y1,-Y2,-Y3). Controls were cultured for 8days without predators (C2, C3). Tails from tadpoles after 8days of each treatment were dissected for RNA extraction and gene expression analysis using Affymetrix Xenopus Genechip arrays.
2016-10-24 | E-GEOD-33250 | biostudies-arrayexpress
Project description:Tadpoles of the anuran species Rana pirica can undergo predator-specific morphological responses. Exposure to a predation threat by larvae of the salamander Hynobius retardatus results in formation of a bulgy body (bulgy morph) with a higher tail. The objective of the present study was to use Affymetrix Xenopus Genechip to profile gene expression in the tail tissue by different predation threat. Tadpoles of Rana pirica treated with larvae salamander for 8days (brainS1, brainS2, brainS3) were analyzed with triplicate. Controls were cultured for 8days without larvae salamander (brainC1,brainC2,brainC3,brainC4,brainC5,brainC6). Brains from tadpoles after 8days of each treatment were dissected for RNA extraction and gene expression analysis using Affymetrix Xenopus Genechip arrays.
2014-10-26 | E-GEOD-33283 | biostudies-arrayexpress
Project description:Lewy body (LB) pathology and loss of dopaminergic neurons are imprints of Parkinson’s disease (PD). LBs are mainly comprised of alpha-Synuclein (Dijkstra et al., 2014). Strolling detection of LBs in brain regions contribute to progressive construct of PD pathology to which molecular mechanisms are not clear (H. Braak & Del Tredici, 2017). Two key facets of LB formation are protein aggregation via misfolding and transmission of misfoldled proteins to various brain regions, eventually causing neuronal death (Goedert, Spillantini, Del Tredici, & Braak, 2013; Pacelli et al., 2015). Misfolding requires alterations in intracellular physiology (Carbone, Costa, Provensi, Mannaioni, & Masi, 2017; Funes et al., 2014; Guzman et al., 2018; Pacelli et al., 2015) and detection of misfolded proteins in exosomes confirms exosomatic transmission (Ngolab et al., 2017). High levels of neurotropic-factors (Brockmann et al., 2017) and changes in bioenergetics are found in PD patients, these can bring physiological alterations (Smith et al., 2018). En masse, these evidences and hipocampal association with synucleopathies (Flores-Cuadrado, Ubeda-Bañon, Saiz-Sanchez, de la Rosa-Prieto, & Martinez-Marcos, 2016) allowed us to probe other volunerable PD proteins in cell-lysate and exosomal proteomes of bFGF treated hippocampal neurons. Using WPCNA we developed co-expression modules and spotted many PD related proteins; which can act as precursors during diseased or onset stage.
2020-07-21 | PXD015969 | Pride