EC Number   |
General Information |
Reference |
|---|
   2.1.1.187 | malfunction |
a mutant deficient in N1-methylguanine745 modification shows a 40% decreased growth rate in rich media, a drastic reduction in loosely coupled ribosomes, a 20% decreased polypeptide chain elongation rate, and increased resistance to the ribosome binding antibiotic viomycin |
704259 |
| 2.1.1.187 | malfunction |
lack of G745 methylation results in reduced rates of protein synthesis and growth. Addition of recombinant plasmid-encoded rrmA to an rrmA-defficient strain remedies these defects |
441500 |
| 2.1.1.187 | malfunction |
mutant lacking N1-methylation of G745 exhibits increased resistance to viomycin in addition to severe defects of growth characteristics |
441502 |
| 2.1.1.187 | malfunction |
slow growth of the Acinetobacter rlmAI knockout. The growth defect of the Acinetobacter rlmAI knockout is lost during serial passaging of the strain on agar plates. None of the Acinetobacter or Escherichia coli cells tested has regained their ability to methylate G745, and all are thus pseudorevertants. The putative second-site mutations are possibly not rescuing the lack of G745 methylation, but are perhaps compensating for some other function of RlmAI. Cell growth is not dependent on G745 methylation, and the RlmAI methyltransferase therefore has another primary function |
660492 |
