IAI FigSearch
Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
This Article
Right arrow Full Text
Right arrow Full Text (PDF)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Similar articles in this journal
Right arrow Similar articles in PubMed
Right arrow Alert me to new issues of the journal
Right arrow Download to citation manager
Right arrowReprints and Permissions
Right arrow Copyright Information
Right arrow Books from ASM Press
Right arrow MicrobeWorld
Citing Articles
Right arrow Citing Articles via HighWire
Right arrow Citing Articles via Google Scholar
Google Scholar
Right arrow Articles by Glew, M. D.
Right arrow Articles by Walker, I. D.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Glew, M. D.
Right arrow Articles by Walker, I. D.

 Previous Article  |  Next Article 

Infection and Immunity, December 1998, p. 5833-5841, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Expression of the pMGA Genes of Mycoplasma gallisepticum Is Controlled by Variation in the GAA Trinucleotide Repeat Lengths within the 5' Noncoding Regions

Michelle D. Glew,dagger Nina Baseggio, Philip F. Markham, Glenn F. Browning, and Ian D. Walker*

Department of Veterinary Science, The University of Melbourne, Parkville, Victoria, Australia 3052

Received 11 March 1998/Returned for modification 4 June 1998/Accepted 19 August 1998

We analyzed the segment of DNA which contains the expressed pMGA gene from one strain of Mycoplasma gallisepticum in normal (strain S6) cells and in cells in which pMGA1.1 gene expression had ceased as a consequence of in vitro culture in the presence of pMGA1.1-specific antibodies. Sequence analysis of isolates lacking pMGA1.1 expression revealed that this gene, which is typically expressed, exhibited sequence changes within a region 5' to its promoter. Specifically, pMGA1.1+ cells contained a (GAA)12 motif upstream of the promoter, whereas in pMGA1.1- cells the corresponding region contained a (GAA)10 motif; when such cells were grown in medium no longer containing pMGA-specific antibodies, pMGA1.1 was reexpressed and the 5' (GAA)12 motif was restored. Two other genes, pMGA1.9 and pMGA1.2, were also shown to acquire a (GAA)12 motif in clones which expressed these genes. The results imply the evolution by the pMGA genes of M. gallisepticum of a novel transcriptional requirement which facilitates rapid and reversible switches in the pMGA expression pattern.


* Corresponding author. Mailing address: Department of Veterinary Science, The University of Melbourne, Parkville, Victoria, Australia 3052. Phone: 61-3-9344 7352. Fax: 61-3-9344 7374. E-mail: i.walker{at}vet.unimelb.edu.au.

dagger Present address: Institute of Bacteriology and Hygiene, Vienna University of Veterinary Medicine, A-1210, Vienna, Austria.


Infection and Immunity, December 1998, p. 5833-5841, Vol. 66, No. 12
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.



This article has been cited by other articles:




Home Help [Feedback] [For Subscribers] [Archive] [Search] [Contents]
J. Bacteriol. J. Virol. Eukaryot. Cell
Microbiol. Mol. Biol. Rev. Clin. Vaccine Immunol. All ASM Journals

Copyright © 1998 by the American Society for Microbiology. All rights reserved.