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PMID: 2540150 Published · ppublish English Journal Article Research Support, Non-U.S. Gov't

Bacillus licheniformis alpha-amylase gene, amyL, is subject to promoter-independent catabolite repression in Bacillus subtilis.

Journal of bacteriology ·Vol. 171 ·No. 5 ·1989-05-00 ·Pages 2435-42

Laoide BM, Chambliss GH, McConnell DJ

Abstract

Expression of the Bacillus licheniformis alpha-amylase gene, amyL, was temporally activated and subject to catabolite repression both in its natural host and when cloned on a 3.55-kilobase fragment in Bacillus subtilis. A subclone from which the promoter region of amyL and sequences upstream from the promoter were deleted had a low level of amylase activity. Expression of the promoterless gene was still subject to repression by glucose when the gene was present either on a multicopy plasmid or integrated into the B. subtilis chromosome. Catabolite repression occurred independently of the amylase promoter and irrespective of the distance of the promoterless amyL gene from the promoter which transcribed it. The transcriptional start sites of amyL activated by its own promoter and by a vector sequence promoter were determined by S1 mapping. alpha-Amylase-specific mRNA levels were measured in repressing and nonrepressing media, and catabolite repression was found to act at the level of transcription.

MeSH Terms
Bacillus/genetics Bacillus subtilis/genetics Base Sequence Blotting, Northern Endonucleases/pharmacology Enzyme Repression Gene Expression Regulation Molecular Sequence Data Promoter Regions, Genetic RNA, Messenger/genetics Single-Strand Specific DNA and RNA Endonucleases Transcription, Genetic alpha-Amylases/genetics
Chemicals
RNA, Messenger Endonucleases Single-Strand Specific DNA and RNA Endonucleases alpha-Amylases
Authors & Affiliations
3 authors, click to expand affiliations / ORCID
Laoide B M
Department of Genetics, Trinity College, University of Dublin, Ireland.
Chambliss G H
McConnell D J
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Article Info
Journal
Journal of bacteriology
Abbr.
J Bacteriol
ISSN
0021-9193
Published
1989-05-00
Pages
2435-42
Language
English
Region
United States
NLM ID
2985120R
PMCID
PMC209918
Subset
IM
Databases
GENBANK
M26412
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