INDUCTION OF ERMC REQUIRES TRANSLATION OF THE LEADER PEPTIDE
INDUCTION OF ERMC REQUIRES TRANSLATION OF THE LEADER PEPTIDE
复制标题
DOI:
10.1002/j.1460-2075.1985.tb03661.x
复制
发表时间:
1985-01-01
期刊:
影响因子:
11.4
通讯作者:
DUBNAU, D
中科院分区:
文献类型:
--
作者:
DUBNAU, D
ermC confers resistance to macrolide-lincosamide streptogramin B antibiotics by specifying a ribosomal RNA methylase, which results in decreased ribosomal affinity for these antibiotics. ermC expression is induced by exposure to erythromycin. A translational regulation model was proposed in which erythromycin causes stalling of a ribosome, which is translating a leader peptide. Stalling causes a conformation shift in the ermC mRNA which in turn unmasks the methylase ribosomal binding site. A prediction of this translational attenuation model for ermC induction was tested by replacing the second codon of the putative ermC leader peptide coding region by TAA. As expected, the introduction of this mutation resulted in an uninducible phenotype which was suppressible by 2 ochre suppressor mutations in Bacillus subtilis. It is concluded that translation through the leader peptide coding region, in frame with the predicted leader peptide, is required for ermC induction.