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Ribosomal RNA methyltransferases contribute to Staphylococcus aureus virulence
Author(s) -
Kyuma Tatsuhiko,
Kimura Satoshi,
Hanada Yuichi,
Suzuki Tsutomu,
Sekimizu Kazuhisa,
Kaito Chikara
Publication year - 2015
Publication title -
the febs journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.981
H-Index - 204
eISSN - 1742-4658
pISSN - 1742-464X
DOI - 10.1111/febs.13302
Subject(s) - methyltransferase , 23s ribosomal rna , ribosomal rna , biology , staphylococcus aureus , virulence , methylation , microbiology and biotechnology , ribosomal protein , ribosome , gene , genetics , rna , bacteria
Post‐transcriptional modifications in r RNA , such as methylation, are observed in functionally important regions of the ribosome. The methyltransferases responsible for these modifications work as housekeeping enzymes to fine‐tune ribosomal function, and the roles of some methyltransferases become more evident under stress conditions. Recently, the 16S r RNA methyltransferases RsmI and RsmH, which are responsible for cytidine dimethylation at the decoding center of the ribosome, were identified in Escherichia coli . The physiological relevance of the r RNA modification, however, remains obscure. We identified rsmI and rsmH as novel virulence genes in Staphylococcus aureus using a silkworm infection model. These genes induced 2′‐ O ‐ and N 4 ‐methylations, respectively, of m 4 Cm1412 of S. aureus 16S r RNA . Deletion of either rsmI or rsmH in S. aureus attenuated the virulence of S. aureus in silkworms, and led to its sensitivity to oxidative stress. Dual luciferase assay revealed that the double‐knockout strain exhibited decreased translational fidelity under oxidative stress conditions. In addition, administration of N ‐acetyl‐ l ‐cysteine, a free‐radical scavenger, restored the killing ability of the double‐knockout strain against silkworms. These findings suggest that the methyl‐modifications of cytidine at position 1412 in 16S r RNA contribute to S. aureus animal killing by conferring resistance to oxidative stress in host animals.