Expression of Mycobacterium tuberculosis NLPC/p60 family protein Rv0024 induce biofilm formation and resistance against cell wall acting anti-tuberculosis drugs in Mycobacterium smegmatis

Padhi, Avinash; Naik, Sumanta Kumar; Sengupta, Srabasti; Ganguli, Geetanjali; Sonawane, Avinash

doi:10.1016/j.micinf.2015.11.007

Cited by 24 publications

(16 citation statements)

References 51 publications

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“…Several studies including our previous work have used Msm as a surrogate model to study the role of various Mtb proteins in pathogenesis [30][31][32][33][34]. The qRT-PCR analysis confirmed that LprE is ectopically expressed in Msm strain grown under in-vitro condition (Fig 2B).…”

Section: Deletion Of Lpre In M Tuberculosis Cdc1551 Decreased Bactersupporting

confidence: 52%

Mycobacterium tuberculosis LprE enhances bacterial persistence by inhibiting cathelicidin and autophagy in macrophages

Padhi

Bhagyaraj

et al. 2017

Preprint

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Section: Deletion Of Lpre In M Tuberculosis Cdc1551 Decreased Bactersupporting

confidence: 52%

Mycobacterium tuberculosis LprE enhances bacterial persistence by inhibiting cathelicidin and autophagy in macrophages

Padhi

Bhagyaraj

et al. 2017

Preprint

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“…In Mycobacterium tuberculosis, the protein Rv0024 has been shown to be involved in biofilm formation. Those biofilms have been found to be resistant to cell wall-acting anti-TB drugs [68]. Still, M. tuberculosis, a mutant lacking the NLPC_P60 protein, is more sensitive to antibiotics and lysozymes, leading to a decrease in the survival in macrophages [69], and the Rv2190c protein is required not only for cell wall maintenance but also for virulence since a mutant is less virulent in a mice model of infection in vivo [70].…”

Section: Discussionmentioning

confidence: 99%

Structural Modeling of Cell Wall Peptidase CwpFM (EntFM) Reveals Distinct Intrinsically Disordered Extensions Specific to Pathogenic Bacillus cereus Strains

Tran

Cormontagne

Vidić

et al. 2020

Toxins

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The emergence of B. cereus as an opportunistic food-borne pathogen has intensified the need to distinguish strains of public health concern. The heterogeneity of the diseases associated with B. cereus infections emphasizes the versatility of these bacteria strains to colonize their host. Nevertheless, the molecular basis of these differences remains unclear. Several toxins are involved in virulence, particularly in gastrointestinal disorders, but there are currently no biological markers able to differentiate pathogenic from harmless strains. We have previously shown that CwpFM is a cell wall peptidase involved in B. cereus virulence. Here, we report a sequence/structure/function characterization of 39 CwpFM sequences, chosen from a collection of B. cereus with diverse virulence phenotypes, from harmless to highly pathogenic strains. CwpFM is homology-modeled in silico as an exported papain-like endopeptidase, with an N-terminal end composed of three successive bacterial Src Homology 3 domains (SH3b1–3) likely to control protein–protein interactions in signaling pathways, and a C-terminal end that contains a catalytic NLPC_P60 domain primed to form a competent active site. We confirmed in vitro that CwpFM is an endopeptidase with a moderate peptidoglycan hydrolase activity. Remarkably, CwpFMs from pathogenic strains harbor a specific stretch of twenty residues intrinsically disordered, inserted between the SH3b3 and the catalytic NLPC_P60 domain. This strongly suggests this linker as a marker of differentiation between B. cereus strains. We believe that our findings improve our understanding of the pathogenicity of B. cereus while advancing both clinical diagnosis and food safety.

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“…The presence of ciaB , a Campylobacter invasion antigen, may contribute to the high invasion of C. jejuni 1655 (Rivera-Amill and Konkel, 1999 ). The nlpC may play a critical role in initial infection process, adherence to host cells (Padhi et al, 2016 ). The cadF , encoding fibronectin protein, may play an important role on the adhesion and colonization of 1655 in chicken (Konkel et al, 1997 ; Monteville et al, 2003 ).…”

Section: Discussionmentioning

confidence: 99%

Virulence and Genomic Feature of Multidrug Resistant Campylobacter jejuni Isolated from Broiler Chicken

et al. 2016

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The aim of this study was to reveal the molecular mechanism involved in multidrug resistance and virulence of Campylobacter jejuni isolated from broiler chickens. The virulence of six multidrug resistant C. jejuni was determined by in vitro and in vivo methods. The de novo whole genome sequencing technology and molecular biology methods were used to analyze the genomic features associated with the multidrug resistance and virulence of a selected isolate (C. jejuni 1655). The comparative genomic analyses revealed a large number of single nucleotide polymorphisms, deletions, rearrangements, and inversions in C. jejuni 1655 compared to reference C. jejuni genomes. The co-emergence of Thr-86-Ile mutation in gyrA gene, A2075G mutation in 23S rRNA gene, tetO, aphA and aadE genes and pTet plasmid in C. jejuni 1655 contributed its multidrug resistance to fluoroquinolones, macrolides, tetracycline, and aminoglycosides. The combination of multiple virulence genes may work together to confer the relative higher virulence in C. jejuni 1655. The co-existence of mobile gene elements (e.g., pTet) and CRISPR-Cas system in C. jejuni 1655 may play an important role in the gene transfer and immune defense. The present study provides basic information of phenotypic and genomic features of C. jejuni 1655, a strain recently isolated from a chicken displaying multidrug resistance and relatively high level of virulence.

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Expression of Mycobacterium tuberculosis NLPC/p60 family protein Rv0024 induce biofilm formation and resistance against cell wall acting anti-tuberculosis drugs in Mycobacterium smegmatis

Cited by 24 publications

References 51 publications

Mycobacterium tuberculosis LprE enhances bacterial persistence by inhibiting cathelicidin and autophagy in macrophages

Mycobacterium tuberculosis LprE enhances bacterial persistence by inhibiting cathelicidin and autophagy in macrophages

Structural Modeling of Cell Wall Peptidase CwpFM (EntFM) Reveals Distinct Intrinsically Disordered Extensions Specific to Pathogenic Bacillus cereus Strains

Virulence and Genomic Feature of Multidrug Resistant Campylobacter jejuni Isolated from Broiler Chicken

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