Use this URL to cite or link to this record in EThOS:
Title: Pactamycin resistance in Streptomyces
Author: Calcutt, Michael John
ISNI:       0000 0001 3514 2728
Awarding Body: University of Leicester
Current Institution: University of Leicester
Date of Award: 1987
Availability of Full Text:
Access from EThOS:
Access from Institution:
The coupled transcription-translation system previously developed for Streptomyces lividans was modified such that it functioned using purified ribosomal subunits, a crude initiation factor preparation and a high speed supernatant fraction. This system was used to investigate antibiotic resistance mechanisms in two Streptomyces which synthesise inhibitors of translation. Resistance to either pactamycin in Streptomyces pactum or celesticetin in Streptomyces caelestis was due to ribosome modification. In each case, high level resistance was attributed solely to one ribosomal subunit, the 30S subunit of the S. pactum ribosome and the 50S subunit of the S. caelestis ribosome. Shotgun cloning experiments have enabled a pactamycin resistance determinant from S. pactum to be isolated in S. lividans. However, in the original pactamycin resistant clone the plasmid was unstable and in the absence of pactamycin selection pressure, only a deleted form could be recovered. When ribosomes from resistant subclones were analysed, it appeared that a ribosome modification system from S. pactum had been cloned. Ribosome reconstitution studies indicated that a property of 16S rRNA was responsible for resistance. Since the cloned resistance determinant was not homologous to 16S rRNA (as judged by Southern analysis), pactamycin resistance in S. pactum is probably due to post-transcriptional modification of 16S rRNA.
Supervisor: Not available Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available
Keywords: Antibiotic Streptomyces study