Mutations in ppe38 block PE_PGRS secretion and increase virulence of Mycobacterium tuberculosis View Full Text


Ontology type: schema:ScholarlyArticle     


Article Info

DATE

2018-01-15

AUTHORS

Louis S. Ates, Anzaan Dippenaar, Roy Ummels, Sander R. Piersma, Aniek D. van der Woude, Kim van der Kuij, Fabien Le Chevalier, Dulce Mata-Espinosa, Jorge Barrios-Payán, Brenda Marquina-Castillo, Carolina Guapillo, Connie R. Jiménez, Arnab Pain, Edith N. G. Houben, Robin M. Warren, Roland Brosch, Rogelio Hernández-Pando, Wilbert Bitter

ABSTRACT

Mycobacterium tuberculosis requires a large number of secreted and exported proteins for its virulence, immune modulation and nutrient uptake. Most of these proteins are transported by the different type VII secretion systems1,2. The most recently evolved type VII secretion system, ESX-5, secretes dozens of substrates belonging to the PE and PPE families, which are named for conserved proline and glutamic acid residues close to the amino terminus3,4. However, the role of these proteins remains largely elusive1. Here, we show that mutations of ppe38 completely block the secretion of two large subsets of ESX-5 substrates, that is, PPE-MPTR and PE_PGRS, together comprising >80 proteins. Importantly, hypervirulent clinical M. tuberculosis strains of the Beijing lineage have such a mutation and a concomitant loss of secretion5. Restoration of PPE38-dependent secretion partially reverted the hypervirulence phenotype of a Beijing strain, and deletion of ppe38 in moderately virulent M. tuberculosis increased virulence. This indicates that these ESX-5 substrates have an important role in virulence attenuation. Phylogenetic analysis revealed that deletion of ppe38 occurred at the branching point of the ‘modern’ Beijing sublineage and is shared by Beijing outbreak strains worldwide, suggesting that this deletion may have contributed to their success and global distribution6,7. More... »

PAGES

181-188

Journal

TITLE

Nature Microbiology

ISSUE

2

VOLUME

3

Identifiers

URI

http://scigraph.springernature.com/pub.10.1038/s41564-017-0090-6

DOI

http://dx.doi.org/10.1038/s41564-017-0090-6

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1100351854

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/29335553


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363 schema:name Department of Medical Microbiology and Infection Prevention, VU University Medical Center, Amsterdam, The Netherlands
364 Unit for Integrated Mycobacterial Pathogenomics, Institut Pasteur, Paris, France
365 rdf:type schema:Organization
366 grid-institutes:grid.45672.32 schema:alternateName Pathogen Genomics Laboratory, BESE Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia
367 schema:name Pathogen Genomics Laboratory, BESE Division, King Abdullah University of Science and Technology (KAUST), Thuwal, Saudi Arabia
368 rdf:type schema:Organization
 




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