An unusual feature associated with LEE1 P1 promoters in enteropathogenic Escherichia coli (EPEC)
Summary Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the −10, extended −10 and −35 elements of the promoter guides...
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Published in | Molecular microbiology Vol. 83; no. 3; pp. 612 - 622 |
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Main Authors | , , , , , , , |
Format | Journal Article |
Language | English |
Published |
Oxford, UK
Blackwell Publishing Ltd
01.02.2012
Blackwell |
Subjects | |
Online Access | Get full text |
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Abstract | Summary
Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the −10, extended −10 and −35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. |
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AbstractList | Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For
Escherichia coli
RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the −10, extended −10 and −35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the
LEE1
operon in enteropathogenic
Escherichia coli
(EPEC) and found two promoters separated by 10 bp,
LEE1
P1A (+1) and
LEE1
P1B (+10) using various
in vitro
biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighboring
A
s at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under
in vivo
conditions, dominant P1B, but not P1A, was subject to regulation by IHF. Summary Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the −10, extended −10 and −35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the -10, extended -10 and -35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. Transcription start points in bacteria are influenced by the nature of the RNA polymerase-promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing ...70, it is presumed that specific sequence in one or more of the -10, extended -10 and -35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. (ProQuest: ... denotes formulae/symbols omitted.) Summary Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing σ70, it is presumed that specific sequence in one or more of the −10, extended −10 and −35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E. coli and found two promoters separated by 10 bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. Transcription start points in bacteria are influenced by the nature of the RNA polymerase.promoter interaction. For Escherichia coli RNA polymerase holoenzyme containing sigma 70, it is presumed that specific sequence in one or more of the -10, extended -10 and -35 elements of the promoter guides the RNAP to select the cognate start point. Here, we investigated the promoter driving expression of the LEE1 operon in enteropathogenic E.coli and found two promoters separated by 10bp, LEE1 P1A (+1) and LEE1 P1B (+10) using various in vitro biochemical tools. A unique feature of P1B was the presence of multiple transcription starts from five neighbouring As at the initial transcribed region. The multiple products did not arise from stuttering synthesis. Analytical software based on information theory was employed to determine promoter elements. The concentration of the NTP pool altered the preferred transcription start points, albeit the underlying mechanism is elusive. Under in vivo conditions, dominant P1B, but not P1A, was subject to regulation by IHF. |
Author | Shin, Minsang Rhee, Joon Haeng Kim, Kun-Hee Schneider, Thomas D. Jeong, Jae-Ho Hong, Yeongjin Kim, Hyun-Ju Choy, Hyon E. |
AuthorAffiliation | 1 Center for Host Defense against Enteropathogenic Bacteria Infection, Chonnam National University Medical School, Kwangju 501-746, South Korea 3 National Cancer Institute, National Institutes of Health, Gene Regulation and Chromosome Biology Laboratory, Building 539, Room 129A, NCI-Frederick, Maryland, United States 2 Department of Microbiology, Chonnam National University Medical School, Kwangju 501-746, South Korea |
AuthorAffiliation_xml | – name: 2 Department of Microbiology, Chonnam National University Medical School, Kwangju 501-746, South Korea – name: 3 National Cancer Institute, National Institutes of Health, Gene Regulation and Chromosome Biology Laboratory, Building 539, Room 129A, NCI-Frederick, Maryland, United States – name: 1 Center for Host Defense against Enteropathogenic Bacteria Infection, Chonnam National University Medical School, Kwangju 501-746, South Korea |
Author_xml | – sequence: 1 givenname: Jae-Ho surname: Jeong fullname: Jeong, Jae-Ho organization: Center for Host Defense against Enteropathogenic Bacteria Infection – sequence: 2 givenname: Hyun-Ju surname: Kim fullname: Kim, Hyun-Ju organization: Center for Host Defense against Enteropathogenic Bacteria Infection – sequence: 3 givenname: Kun-Hee surname: Kim fullname: Kim, Kun-Hee organization: Center for Host Defense against Enteropathogenic Bacteria Infection – sequence: 4 givenname: Minsang surname: Shin fullname: Shin, Minsang organization: Center for Host Defense against Enteropathogenic Bacteria Infection – sequence: 5 givenname: Yeongjin surname: Hong fullname: Hong, Yeongjin organization: Center for Host Defense against Enteropathogenic Bacteria Infection – sequence: 6 givenname: Joon Haeng surname: Rhee fullname: Rhee, Joon Haeng organization: Department of Microbiology, Chonnam National University Medical School, Kwangju 501-746, South Korea – sequence: 7 givenname: Thomas D. surname: Schneider fullname: Schneider, Thomas D. organization: National Cancer Institute, National Institutes of Health, Gene Regulation and Chromosome Biology Laboratory, Building 539, Room 129A, NCI-Frederick, Maryland, USA – sequence: 8 givenname: Hyon E. surname: Choy fullname: Choy, Hyon E. email: hyonchoy@jnu.ac.kr organization: Center for Host Defense against Enteropathogenic Bacteria Infection |
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Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase... Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme... Summary Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase... Transcription start points in bacteria are influenced by the nature of the RNA polymerase-promoter interaction. For Escherichia coli RNA polymerase holoenzyme... Transcription start points in bacteria are influenced by the nature of the RNA polymerase.promoter interaction. For Escherichia coli RNA polymerase holoenzyme... Transcription start points in bacteria are influenced by the nature of the RNA polymerase·promoter interaction. For Escherichia coli RNA polymerase holoenzyme... |
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SubjectTerms | Bacteriology Base Sequence Biochemistry Biological and medical sciences Biosynthesis E coli Enteropathogenic Escherichia coli - genetics Escherichia coli Escherichia coli Proteins - genetics Fundamental and applied biological sciences. Psychology Gene expression Gene Expression Regulation, Bacterial Microbiology Miscellaneous Molecular Sequence Data Operon Promoter Regions, Genetic RNA polymerase Software Trans-Activators - genetics Transcription Initiation Site Transcription, Genetic |
Title | An unusual feature associated with LEE1 P1 promoters in enteropathogenic Escherichia coli (EPEC) |
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