Dataset Information

Impact of carbon source supplementations on Pseudomonas aeruginosa physiology

ABSTRACT: By a global proteomic approach and phenotypic assays, we investigated the impact of various carbon source supplementations (glucose, glutamate, succinate and citrate) on the physiology P. aeruginosa PA14 strain. A total of 581 proteins were identified as differentially expressed in the 4 conditions. Most of them were more abundant in citrate supplementation and were involved in virulence, motility, biofilm development and antibiotic resistance.

INSTRUMENT(S): Q Exactive

ORGANISM(S): Pseudomonas Aeruginosa Pa14

SUBMITTER: Julie Hardouin

LAB HEAD: Julie Hardouin

PROVIDER: PXD030421 | Pride | 2022-05-08

REPOSITORIES: Pride

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Dataset's files

Source:

			Action	DRS
	GAVIARD_20170524_filtresstrictes_excel.xlsx	Xlsx
	PA14_Extra_Citrate_1_01.raw	Raw
	PA14_Extra_Citrate_2_01.raw	Raw
	PA14_Extra_Citrate_3_01.raw	Raw
	PA14_Extra_Citrate_4_01.raw	Raw

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Impact of Carbon Source Supplementations on Pseudomonas aeruginosa Physiology.

Sauvage Salomé S Gaviard Charlotte C Tahrioui Ali A Coquet Laurent L Le Hung H Alexandre Stéphane S Ben Abdelkrim Ahmed A Bouffartigues Emeline E Lesouhaitier Olivier O Chevalier Sylvie S Jouenne Thierry T Hardouin Julie J

Journal of proteome research 20220428 6

Pseudomonas aeruginosa is an opportunistic pathogen highly resistant to a wide range of antimicrobial agents, making its infections very difficult to treat. Since microorganisms need to perpetually adapt to their surrounding environment, understanding the effect of carbon sources on P. aeruginosa physiology is therefore essential to avoid increasing drug-resistance and better fight this pathogen. By a global proteomic approach and phenotypic assays, we investigated the impact of va ...[more]

PMID: 35482949

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Project description:P. aeruginosa is the leading cause of death in patients with cystic fibrosis patients and one of the most problematic bacterial pathogens responsible for hospital-acquired infections. This pathogen has a high capacity to form biofilms on inert and living surfaces. This lifestyle allows it to persist in various hospital niches or on medical device which become vectors of contamination. Chronic infections are extremely complicated to eradicate due to the remarkable antimicrobial resistance of biofilms leading to a persistence in the tissue and an immune system exhaustion. It is therefore becoming essential to understand the mechanisms of biofilm formation to find new therapeutic targets in order to develop effective antibiofilm strategies. We previously identified in P. aeruginosa PA01 biofilms an accumulation of a hypothetical protein named PA3731 and its deletion impacted the biofilm formation. Similarly, to PspA, a protein from the well-known Psp system of E. coli, PA3731 is a has a predicted structure mostly helical, a PspA/IM30 domain and was accumulated during an osmotic shock. In P. aeruginosa genome, PA3731 appears to form a cluster with 3 genes (PA3732 to PA3729) that we named BAC system for “Biofilm Associated Cluster”. Here we worked on the PA14 strain and focus our study on PA14_16140, the PA3732 homologue. Using a ∆16140 mutant and phenotypic approach, we confirmed the role of the BAC system in the virulence and biofilm formation. We added supplementary genes coding the BAC system and demonstrate that altogether they form an operonic structure regulates by RpoN. We get further insight the role PA14_16140 by proteomic quantitative approach revealing an accumulation of the BAC system proteins in ∆16140 biofilms suggesting its regulatory role of the bac operon. Moreover, we present here the first crystallographic structure of PA14_16140. To summarise, according to our studies, and although further analysis is still required, this newly discovered operon appears composed firstly of its regulator and then of a homologous PspA.

Dataset Information

Impact of carbon source supplementations on Pseudomonas aeruginosa physiology

Dataset's files

Publications

Impact of Carbon Source Supplementations on <i>Pseudomonas aeruginosa</i> Physiology.

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