Dataset Information

Proteomic study of Acinetobacter johnsonii JH7 under Sb(III) stress

ABSTRACT: Antimony (Sb) pollution, especially released from mining activities has already been widely recognized as a global concern. To gauge strategies for the remediation of an Sb-contaminated ecosystem, the exploration of native microbiota Sb(III) resistance mechanism is of great significance. Acinetobacter is one of the bacterial genera abundantly thriving in Sb(III)-contaminated environments, the scientific elaboration of Sb(III)-resistance mechanisms of Acinetobacter is imperative. Proteomics experiment was performed (Acinetobacter johnsonii JH7 with and without Sb(III) addtion) to probe its pattern of proteins change under Sb(III) stress. We hope that the mechanisms of Sb(III) resistance of Acinetobacter could be revealed by using iTRAQ this time.

ORGANISM(S): Acinetobacter Johnsonii

SUBMITTER: Jihai Gu

PROVIDER: PXD017203 | iProX | Mon Jan 20 00:00:00 GMT 2020

REPOSITORIES: iProX

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Comprehensive genomic and proteomic profiling reveal Acinetobacter johnsonii JH7 responses to Sb(III) toxicity.

Gu Jihai J Yao Jun J Duran Robert R Sunahara Geoffrey G

The Science of the total environment 20200725

Antimony (Sb) pollution poses a severe health threat to ecosystems. However, the toxic effects of Sb on biota are far from being elucidated. One of the unresolved questions is the molecular signal pathways underlying microbial adaptation to excess antimonite or Sb(III) exposure. The response of a Sb(III)-resistant bacterium Acinetobacter. johnsonii JH7 to Sb(III) stress was investigated using genomic and proteomic profiling. Sb(III) induced the formation of reactive oxygen species thereby leadin ...[more]

PMID: 32805562

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Project description:Claret2009 - Predicting phase III overall survival in colorectal cancer This model is described in the article: Model-based prediction of phase III overall survival in colorectal cancer on the basis of phase II tumor dynamics. Claret L, Girard P, Hoff PM, Van Cutsem E, Zuideveld KP, Jorga K, Fagerberg J, Bruno R. J. Clin. Oncol. 2009 Sep; 27(25): 4103-4108 Abstract: PURPOSE: We developed a drug-disease simulation model to predict antitumor response and overall survival in phase III studies from longitudinal tumor size data in phase II trials. METHODS: We developed a longitudinal exposure-response tumor-growth inhibition (TGI) model of drug effect (and resistance) using phase II data of capecitabine (n = 34) and historical phase III data of fluorouracil (FU; n = 252) in colorectal cancer (CRC); and we developed a parametric survival model that related change in tumor size and patient characteristics to survival time using historical phase III data (n = 245). The models were validated in simulation of antitumor response and survival in an independent phase III study (n = 1,000 replicates) of capecitabine versus FU in CRC. RESULTS: The TGI model provided a good fit of longitudinal tumor size data. A lognormal distribution best described the survival time, and baseline tumor size and change in tumor size from baseline at week 7 were predictors (P < .00001). Predicted change of tumor size and survival time distributions in the phase III study for both capecitabine and FU were consistent with observed values, for example, 431 days (90% prediction interval, 362 to 514 days) versus 401 days observed for survival in the capecitabine arm. A modest survival improvement of 39 days (90% prediction interval, -21 to 110 days) versus 35 days observed was predicted for capecitabine. CONCLUSION: The modeling framework successfully predicted survival in a phase III trial on the basis of capecitabine phase II data in CRC. It is a useful tool to support end-of-phase II decisions and design of phase III studies. This model is hosted on BioModels Database and identified by: MODEL1708310001. To cite BioModels Database, please use: BioModels Database: An enhanced, curated and annotated resource for published quantitative kinetic models. To the extent possible under law, all copyright and related or neighbouring rights to this encoded model have been dedicated to the public domain worldwide. Please refer to CC0 Public Domain Dedication for more information.

Project description:Our interest lies in how plants respond to bacterial pathogens. Over the past three years we have identified and documented reproducible, landmark biochemical and molecular events following the challenge of Arabidopsis with the phytopathogenic enterobacteria P. syringae. Significantly, our studies revealed 60% of cDNA-AFLP differentials not present on the 8,200 feature GeneChips and 20% absent from public EST databases (de Torres in press). We now seek to exploit this background using carefully defined time-points to analyse global changes in the Arabidopsis transcriptome using challenges selected to define gene targets implicated in (i) expression of basal immunity (ii) the establishment of successful parasitism (resistance) by a virulent pathogen (host). The results will provide a rationale for future functional assays of the identified pathways using transgenic knockouts and mutant analyses. Additionally, data will provide underpinning support for comparative proteomics of the defense response currently in progress with GARNet support using the same experimental parameters (BBSRC 32/P14635). We propose the following treatments: (i) Mock vs. DC3000hrpA @ 60 min: 60 minutes is subsequent to host immediate-early stress responses and will catalogue the innate responses induced by pathogen associated molecular patterns. The hrpA lesion will ensure no type III effectors influence transcriptional responses. Gene products induced at this time are predicted to potentiate latter host responses (2 treatments X 3 biological replicates = 6 chips). (ii) Mock vs. DC3000 vs. DC3000hrpA vs. DC3000::avrRpm1 @ 4 hours: A key time point previously defined where no macroscopic symptoms are visible but significant differences exist between compatible and incompatible interactions at the molecular and physiological levels. These treatments will serve to define the earliest genes induced by the complement of DC3000 type III effector and will specifically define genes/pathways suppressed by virulence factors in addition to those implicated in orchestration of the hypersensitive cell death. We will also include an incompatible interaction on a transgenic line expressing an RPM1 interacting protein, which fails to mount an HR but exhibits hyper-resistance. We predict this challenge will separate the resistance response (pathogen restriction) from that associated with hypersensitive cell death (5 treatments X 3 biological replicates = 15 chips). (iii) Mock vs. DC3000 vs. DC3000hrpA @ 14 hours: At 10 h before phenotypes are apparent in the DC3000 background, Type III effector delivery is well advanced and impact on host transcription maximal (3 treatments X 3 biological replicates = 9 chips). Keywords: time_series_design; pathogenicity_design; compound_treatment_design

Dataset Information

Proteomic study of Acinetobacter johnsonii JH7 under Sb(III) stress

Publications

Comprehensive genomic and proteomic profiling reveal Acinetobacter johnsonii JH7 responses to Sb(III) toxicity.

Similar Datasets

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