Skip Navigation

This Article
Right arrow Print PDF (2656K)
Right arrow Alert me when this article is cited
Right arrow Alert me if a correction is posted
Services
Right arrow Email this article to a friend
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 Add to My Personal Archive
Right arrow Download to citation manager
Right arrow Search for citing articles in:
ISI Web of Science (33)
Right arrow Commercial Re-use Guidelines
for Open Access NAR Content
Google Scholar
Right arrow Articles by Piper, P.W.
Right arrow Articles by Kingsman, S.M.
Right arrow Search for Related Content
PubMed
Right arrow PubMed Citation
Right arrow Articles by Piper, P.W.
Right arrow Articles by Kingsman, S.M.
Social Bookmarking
 Add to CiteULike   Add to Connotea   Add to Del.icio.us  
What's this?

Nucleic Acids Research, 1988, Vol. 16, No. 4 1333-1348
© 1988


Articles

A heat shock element in the phosphoglycerate kinase gene promoter of yeast

P.W. Piper*, B. Curran, M.W. Davies, K. Hirst, A. Lockheart, J.E. Ogden1,+, C.A. Stanway1, A.J. Kingsman1 and S.M. Kingsman1

Department of Biochemistry, University College London Gower Street, London WC1E 6BT 1Department of Biochemistry, University of Oxford Oxford OX1 3QU, UK

*To whom correspondence should be addressed

Received November 23, 1987. Revised January 11, 1988. Accepted January 11, 1988.

The phosphoglycerate kinase (PGK) promoter is often employed in yeast expression vectors due to its very high efficiency. Its activity in unstressed cells has been shown to be due to an upstream activator site (UASPGK) at –402 to –479. Since levels of PGK mRNA can sometimes be elevated by heat shock of yeast cultures this investigation determined how specific deletions of PGK promoter sequences affect levels of PGK mRNA both before and after heat shock. A series of PGK promoter deletions was inserted on a high copy plasmid into cells having a TRP1 gene disruption of the solitary chromosomal PGK locus. This enabled PGK transcripts of plasmid and chromosomal origin to be distinguished by virtue of their different sizes. Certain deletions lacking UAS PGK displayed activities that were very low in unstressed cells, but which increased fifty to one-hundred fold after heat shock. With UAS PGK present heat shock had only a relatively small or negligible effect on PGK mRNA levels. Heat shock activation was abolished when the –256 to –377 region with homology to the heat shock element consensus of eukaryotes was deleted in addition to UASPGK! but was unaffected by the deletion of regions further downstream containing TATA- and CAAT- sequence motifs. This is the first demonstration of a heat shock element, an activator site normally found upstream of eukaryotic heat shock protein genes, as a natural constituent of a high efficiency glycolytic promoter. It is proposed that PGK may be one member of a small subset of yeast genes that are highly expressed in unstressed cells yet possess a heat shock element to ensure their continued transcription after heat shock.


+Present address: Delta Biotechnology Ltd, Castle Court, Castle Boulevard, Nottingham NG7 1FD, UK


Add to CiteULike CiteULike   Add to Connotea Connotea   Add to Del.icio.us Del.icio.us    What's this?


This article has been cited by other articles:


Home page
MicrobiologyHome page
A. K. Pearce, K. Crimmins, E. Groussac, M. J. E. Hewlins, J. R. Dickinson, J. Francois, I. R. Booth, and A. J. P. Brown
Pyruvate kinase (Pyk1) levels influence both the rate and direction of carbon flux in yeast under fermentative conditions
Microbiology, February 1, 2001; 147(2): 391 - 401.
[Abstract] [Full Text]



Disclaimer:
Please note that abstracts for content published before 1996 were created through digital scanning and may therefore not exactly replicate the text of the original print issues. All efforts have been made to ensure accuracy, but the Publisher will not be held responsible for any remaining inaccuracies. If you require any further clarification, please contact our Customer Services Department.