Dataset Information

Comparison of Proteomic Responses

ABSTRACT: To facilitate antibiotic research, we have developed a compendium of proteomic responses that allows rapid classification of compounds into those with precedented and unprecedented modes of action. We gathered more than 100 proteomic response profiles of B. subtilis to treatment with antibiotics. To depict acute bacterial responses to sublethal doses of antibiotics, we used pulse-labeling of proteins that are newly synthesized after antibiotic challenge and analyze the proteome by 2D-PAGE. Subsequently, marker proteins were excised from non-radioactive gels and identified by mass spectrometry. Through compilation of response profiles, marker proteins are delineated as signatures, which are specific for inhibition of cellular processes like DNA, RNA, or protein biosynthesis, metabolic processes like fatty acid or folic acid biosynthesis, and attacks on cellular structures like the cytoplasmic membrane or the cell wall.

INSTRUMENT(S): Synapt MS

ORGANISM(S): Bacillus Subtilis Subsp. Subtilis Str. 168

SUBMITTER: Sina Schäkermann

LAB HEAD: Prof. Dr. Julia Bandow

PROVIDER: PXD011640 | Pride | 2020-10-01

REPOSITORIES: Pride

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Project description:Tan2012 - Antibiotic Treatment, Inoculum Effect The efficacy of many antibiotics decreases with increasing bacterial density, a phenomenon called the ‘inoculum effect’ (IE). This study reveals that, for ribosome-targeting antibiotics, IE is due to bistable inhibition of bacterial growth, which reduces the efficacy of certain treatment frequencies. This model is described in the article: The inoculum effect and band-pass bacterial response to periodic antibiotic treatment. Tan C, Phillip Smith R, Srimani JK, Riccione KA, Prasada S, Kuehn M, You L. Mol Syst Biol. 2012 Oct 9; 8:617 Abstract: The inoculum effect (IE) refers to the decreasing efficacy of an antibiotic with increasing bacterial density. It represents a unique strategy of antibiotic tolerance and it can complicate design of effective antibiotic treatment of bacterial infections. To gain insight into this phenomenon, we have analyzed responses of a lab strain of Escherichia coli to antibiotics that target the ribosome. We show that the IE can be explained by bistable inhibition of bacterial growth. A critical requirement for this bistability is sufficiently fast degradation of ribosomes, which can result from antibiotic-induced heat-shock response. Furthermore, antibiotics that elicit the IE can lead to 'band-pass' response of bacterial growth to periodic antibiotic treatment: the treatment efficacy drastically diminishes at intermediate frequencies of treatment. Our proposed mechanism for the IE may be generally applicable to other bacterial species treated with antibiotics targeting the ribosomes. This model is hosted on BioModels Database and identified by: MODEL1208300000 . 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.

Dataset Information

Comparison of Proteomic Responses

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