In the first step of this cycle, the SAM-dependent
methylases that use SAM as a substrate produce S-adenosyl homocysteine as a product.
The resistance is via three related genes, ermA, ermB, and ermC, which produce
methylases that alter the targeted ribosome by methylating it.
Also plasmid-mediated
methylases that cause resistance to all aminoglycosides have been encountered.
Site-specific
methylases induce the SOS DNA repair response in Escherichia coli.
The activity of endogenous
methylases in human placenta increased steadily with weeks of gestation, suggesting that increased formation of methyltransferases might occur during pregnancy (Paik et al.
24,25) Secondly, high-level macrolide resistance may result from modification of the drug target (ribosomal binding site) via erm(B) genes that encode 23S rRNA
methylases, and lead to cross-resistance to the ML[S.
Like other
methylases, Dam chemically coats DNA with clusters of atoms known as methyl groups.
In that study, ~2-5% of CCGG sites were fully methylated, suggesting that nuclear
methylases enter a subset of the mitochondria.
Enzymes in Genetic Engineering: Restriction Endonucleases and
Methylases16S rRNA
methylases were found to confer high levels of resistance to aminoglycosides such as amikacin, tobramycin, and gentamicin.
Composite transposons and other genetic determinants also considered to be located in specific mobile elements such as macrolide (either encoding
methylases [erm genes] or efflux pumps [mef genes]) and tetracycline resistance determinants (tet genes) have been found among streptococcal species of human origin.
These mechanisms include target site modification by
methylases encoded by erm genes, in particular erm(A), erm(B), and erm(C).
