Open AccessDeletion of the Zinc Transporter Lipoprotein AdcAII Causes Hyperencapsulation of Streptococcus pneumoniae Associated with Distinct Alleles of the Type I Restriction-Modification System
Author(s) -
Claire Durmort,
Giuseppe Ercoli,
Elisa RamosSevillano,
Suneeta Chimalapati,
Richard D. Haigh,
Megan De Ste Croix,
Katherine A. Gould,
Jason Hinds,
Yann Guérardel,
Thierry Vernet,
Marco R. Oggioni,
Jeremy S. Brown
Publication year - 2020
Publication title -
mbio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.562
H-Index - 121
eISSN - 2161-2129
pISSN - 2150-7511
DOI - 10.1128/mbio.00445-20
Subject(s) - biology , streptococcus pneumoniae , bacterial capsule , genetics , mutant , allele , locus (genetics) , phenotype , gene , wild type , restriction fragment length polymorphism , virulence , genotype , microbiology and biotechnology , bacteria
The Streptococcus pneumoniae capsule affects multiple interactions with the host including contributing to colonization and immune evasion. During infection, the capsule thickness varies, but the mechanisms regulating this are poorly understood. We have identified an unsuspected relationship between mutation of adcAII , a gene that encodes a zinc uptake lipoprotein, and capsule thickness. Mutation of adcAII resulted in a striking hyperencapsulated phenotype, increased resistance to complement-mediated neutrophil killing, and increased S. pneumoniae virulence in mouse models of infection. Transcriptome and PCR analysis linked the hyperencapsulated phenotype of the ΔadcAII strain to specific alleles of the SpnD39III (ST5556II) type I restriction-modification system, a system which has previously been shown to affect capsule thickness. Our data provide further evidence for the importance of the SpnD39III (ST5556II) type I restriction-modification system for modulating capsule thickness and identify an unexpected link between capsule thickness and ΔadcAII , further investigation of which could further characterize mechanisms of capsule regulation.