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Contribution of a ZIP‐family protein to manganese uptake and infective endocarditis virulence in Streptococcus sanguinis
Author(s) -
Puccio Tanya,
Kunka Karina S.,
An SeonSook,
Kitten Todd
Publication year - 2022
Publication title -
molecular microbiology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.857
H-Index - 247
eISSN - 1365-2958
pISSN - 0950-382X
DOI - 10.1111/mmi.14853
Subject(s) - virulence , mutant , biology , streptococcus sanguinis , microbiology and biotechnology , endocarditis , phenotype , gene , transporter , genetics , bacteria , streptococcus mutans , medicine , surgery
Streptococcus sanguinis is an important cause of infective endocarditis. In strain SK36, the ABC‐family manganese transporter, SsaACB, is essential for virulence. We have now identified a ZIP‐family protein, TmpA, as a secondary manganese transporter. A tmpA mutant had no phenotype, but a Δ ssaACB Δ tmpA mutant was more attenuated for serum growth and for virulence in a rabbit model than its Δ ssaACB parent. The growth of both mutants was restored by supplemental manganese, but the Δ ssaACB Δ tmpA mutant required twenty‐fold more and accumulated less. Although ZIP‐family proteins are known for zinc and iron transport, TmpA‐mediated transport of either metal was minimal. While ssaACB appears ubiquitous in St. sanguinis , tmpA was present in a majority of strains and a mntH gene encoding an NRAMP‐family transporter was identified in relatively few, including VMC66. As in SK36, deletion of ssaACB greatly diminished VMC66 endocarditis virulence and serum growth, and deletion of tmpA from this mutant diminished virulence further. Virulence was not significantly altered by deletion of mntH from either VMC66 or its Δ ssaACB mutant. This and the accompanying paper together suggest that SsaACB is of primary importance for endocarditis virulence while secondary transporters TmpA and MntH contribute to growth under differing conditions.