Transposon screen for PARylation targets
Ontology highlight
ABSTRACT:
PROVIDER: PRJEB26343 | ENA |
REPOSITORIES: ENA
Similar Datasets
Project description:A PiggyBac transposon based screen in a murine pancreatic cancer model.This data has been described in the following article [doi:10.1038/ng.3164] and its further analysis can be freely submitted for publication. For information on the proper use of data shared by the Wellcome Trust Sanger Institute (including information on acknowledgement), please see http://www.sanger.ac.uk/datasharing/
2016-07-04 | E-ERAD-514 | biostudies-arrayexpress
Project description:Microarray Tracking of transposon mutants for a H. pylori mouse colonization screen described in Baldwin DN et al. 2007, I&I, 75(2):??, doi:10.1128/IAI.01176-06. Screen in NSH57 H. pylori strain background. Original 50,000 clone transposon library was plated and patched to make 25 pools of 48 clones. Clones were infected into 4-8 C57Bl/6 mice and stomach bacteria from at least two mice were harvested at 1 week or one month. Semi-random PCR was used to amplify and label the DNA next to the transposon insertion from the input (Cy3) and output pool (Cy5) genomic DNA for each array. Two arrays were done per mouse. One array labeled from the left side of transposon (primers S, 2C) and one array labeled from the right side of the transposon (primers N3, 2C). Transposon insertions were defined by spots with signal four standard deviations above background in both arrays. We also counted insertions where two adjacent gene spots (after arranging the data in genome order) gave signal from the two different sides of the transposon (but not both).
2006-12-15 | E-SMDB-3900 | biostudies-arrayexpress
Project description:Microarray Tracking of transposon mutants for a H. pylori mouse colonization screen described in Baldwin DN et al. 2007, I&I, 75(2):??, doi:10.1128/IAI.01176-06. Screen in NSH79 H. pylori strain background. Original 2000 clone transposon library was plated and patched to make 25 pools of 48 clones. Clones were infected into 4-8 C57Bl/6 mice and stomach bacteria from at least two mice were harvested at 1 week or one month. Semi-random PCR was used to amplify and label the DNA next to the transposon insertion from the input (Cy3) and output pool (Cy5) genomic DNA for each array. Two arrays were done per mouse. One array labeled from the left side of transposon (primers S, 2C) and one array labeled from the right side of the transposon (primers N3, 2C). Transposon insertions were defined by spots with signal four standard deviations above background in both arrays. We also counted insertions where two adjacent gene spots (after arranging the data in genome order) gave signal from the two different sides of the transposon (but not both).
2006-12-15 | E-SMDB-3901 | biostudies-arrayexpress
Project description:Comprehensive transposon insertion sequencing screen in Francisella tularensis LVS
| PRJNA576682 | ENA
Project description:We used an inhalation mouse model of infection to query a collection of 2149 mutants in a Francisella tularensis subsp. novicida background for genes required for growth, survival and systemic dissemination. A microarray-based genome-wide negative selection screen (Microarray tracking of transposon mutants = MATT) allowed us to monitor the behavior of transposon insertions in 1371 unique genes. Interestingly most of these genes persisted in lung and colonized liver and spleen. We found 44 (35%) genes negatively selected in lung and 81 (65%) genes negatively selected in liver and/or spleen. If negative selection in lung occurred, the attenuated mutants in general persisted at 24h after infection, disseminated to liver and/or spleen and appeared to be lost in lung after 48 to 72h of infection. These genes with a strong phenotype in lung but also potential for dissemination might be attractive vaccine or drug candidates. Keywords: Genome-Wide Negative Selection Screen 185 arrays, no duplicates/replicates Filtered data (per organ/timepoint) provided as a supplementary file
2008-12-30 | E-GEOD-11297 | biostudies-arrayexpress
Project description:A large fraction of our genome consists of mobile genetic elements. Governing transposons in germ cells is critically important, and failure to do so compromises genome integrity, leading to sterility. In animals, the piRNA pathway is the key to transposon constraint, yet the precise molecular details of how piRNAs are formed and how the pathway represses mobile elements remain poorly understood. In an effort to identify general requirements for transposon control and novel components of the piRNA pathway, we carried out a genome-wide RNAi screen in Drosophila ovarian somatic sheet cells. We identified and validated 87 genes necessary for transposon silencing. Among these were several novel piRNA biogenesis factors. We also found CG3893 (asterix) to be essential for transposon silencing, most likely by contributing to the effector step of transcriptional repression. Asterix loss leads to decreases in H3K9me3 marks on certain transposons but has no effect on piRNA levels.
2013-05-09 | GSE46009 | GEO
Project description:We used an inhalation mouse model of infection to query a collection of 2149 mutants in a Francisella tularensis subsp. novicida background for genes required for growth, survival and systemic dissemination. A microarray-based genome-wide negative selection screen (Microarray tracking of transposon mutants = MATT) allowed us to monitor the behavior of transposon insertions in 1371 unique genes. Interestingly most of these genes persisted in lung and colonized liver and spleen. We found 44 (35%) genes negatively selected in lung and 81 (65%) genes negatively selected in liver and/or spleen. If negative selection in lung occurred, the attenuated mutants in general persisted at 24h after infection, disseminated to liver and/or spleen and appeared to be lost in lung after 48 to 72h of infection. These genes with a strong phenotype in lung but also potential for dissemination might be attractive vaccine or drug candidates. Keywords: Genome-Wide Negative Selection Screen
2008-12-31 | GSE11297 | GEO
Project description:Transposon mutagenesis screen in Klebsiella pneumoniae
| PRJEB76649 | ENA
Project description:A large fraction of our genome consists of mobile genetic elements. Governing transposons in germ cells is critically important, and failure to do so compromises genome integrity, leading to sterility. In animals, the piRNA pathway is the key to transposon constraint, yet the precise molecular details of how piRNAs are formed and how the pathway represses mobile elements remain poorly understood. In an effort to identify general requirements for transposon control and novel components of the piRNA pathway, we carried out a genome-wide RNAi screen in Drosophila ovarian somatic sheet cells. We identified and validated 87 genes necessary for transposon silencing. Among these were several novel piRNA biogenesis factors. We also found CG3893 (asterix) to be essential for transposon silencing, most likely by contributing to the effector step of transcriptional repression. Asterix loss leads to decreases in H3K9me3 marks on certain transposons but has no effect on piRNA levels. We sequenced small RNAs, RNA-seq and ChIP-seq from either tj-Gal4 driven hpRNA knockdown flies or P-element insertion flies
2013-05-09 | E-GEOD-46009 | biostudies-arrayexpress
Project description:Genotype directed anti-cancer therapies such BRAF inhibitor in BRAF mutant melanoma can show remarkable clinical efficacy but resistance limits their benefit. We show that a transposon activation screen efficiently identifies resistance genes to BRAF and captures a number of previously uncharacterized resistance mechanisms, including an E3 ubiquitin ligase NEDD4L and the Hippo pathway effector WWTR1 (TAZ). Resistance can be reversed by combining BRAF inhibition with tyrosine kinase inhibitors as observed previously for other resistance genes. Moreover, an integrative analysis of several gain- and loss-of-function genetic screens performed in the same context reveals smaller functional diversity of resistance mechanisms to MAPK inhibition than suggested by the broad range of resistance genes identified, implying common therapeutic strategies. A375 cells with lentiviral vector controls or WWTR1 cDNA plasmid.
2016-07-01 | E-GEOD-73470 | biostudies-arrayexpress