Environmental response and autoregulation of Clostridium difficile TxeR, a sigma factor for toxin gene expression

被引:92
作者
Mani, N
Lyras, D
Barroso, L
Howarth, P
Wilkins, T
Rood, JI
Sonenshein, AL
Dupuy, B
机构
[1] Tufts Univ, Sch Med, Dept Mol Biol & Microbiol, Boston, MA 02111 USA
[2] Monash Univ, Dept Microbiol, Clayton, Vic 3168, Australia
[3] Virginia Tech, Fralin Biotechnol Ctr, Blacksburg, VA 24061 USA
[4] Inst Pasteur, Unite Genet Mol Bacterienne, Paris, France
关键词
D O I
10.1128/JB.184.21.5971-5978.2002
中图分类号
Q93 [微生物学];
学科分类号
071005 ; 100705 ;
摘要
TxeR, a sigma factor that directs Clostridium difficile RNA polymerase to recognize the promoters of two major toxin genes, was shown to stimulate its own synthesis. Whether expressed in C. difficile, Clostridium perfringens, or Escherichia coli, TxeR stimulated transcription of fusions of the txeR promoter region to reporter genes. As is the case for the tox genes, treR expression was responsive to the cellular growth phase and the constituents of the medium. That is, the level of expression in broth culture was low during the exponential growth phase, but rapidly increased as cells approached the stationary phase. In the presence of excess glucose, expression from the txeR promoter was repressed. The results support a model for toxin gene expression in which synthesis of TxeR is induced by specific environmental signals. The increased level of TxeR then permits high-level expression of the toxin genes. The study of txeR gene regulation in C. difficile was made possible by introduction of a mobilizable, replicative plasmid via conjugation with E. coli.
引用
收藏
页码:5971 / 5978
页数:8
相关论文
共 46 条
[1]  
BANNO Y, 1984, REV INFECT DIS, V6, pS11
[2]  
BRADFORD MM, 1976, ANAL BIOCHEM, V72, P248, DOI 10.1016/0003-2697(76)90527-3
[3]   Definition of the single integration site of the pathogenicity locus in Clostridium difficile [J].
Braun, V ;
Hundsberger, T ;
Leukel, P ;
Sauerborn, M ;
vonEichelStreiber, C .
GENE, 1996, 181 (1-2) :29-38
[4]   Analysis of the pathogenicity locus in Clostridium difficile strains [J].
Cohen, SH ;
Tang, YJ ;
Silva, J .
JOURNAL OF INFECTIOUS DISEASES, 2000, 181 (02) :659-663
[5]   NONCHROMOSOMAL ANTIBIOTIC RESISTANCE IN BACTERIA - GENETIC TRANSFORMATION OF ESCHERICHIA-COLI BY R-FACTOR DNA [J].
COHEN, SN ;
CHANG, ACY ;
HSU, L .
PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA, 1972, 69 (08) :2110-&
[6]   MOLECULAR CHARACTERIZATION OF THE CLOSTRIDIUM-DIFFICILE TOXIN-A GENE [J].
DOVE, CH ;
WANG, SZ ;
PRICE, SB ;
PHELPS, CJ ;
LYERLY, DM ;
WILKINS, TD ;
JOHNSON, JL .
INFECTION AND IMMUNITY, 1990, 58 (02) :480-488
[7]   Regulated transcription of Clostridium difficile toxin genes [J].
Dupuy, B ;
Sonenshein, AL .
MOLECULAR MICROBIOLOGY, 1998, 27 (01) :107-120
[8]  
GARNIER T, 1988, MOL MICROBIOL, V2, P607
[9]   THE TOXIGENIC ELEMENT OF CLOSTRIDIUM-DIFFICILE STRAIN VPI-10463 [J].
HAMMOND, GA ;
JOHNSON, JL .
MICROBIAL PATHOGENESIS, 1995, 19 (04) :203-213
[10]   Transcriptional analysis of the toxigenic element of Clostridium difficile [J].
Hammond, GA ;
Lyerly, DM ;
Johnson, JL .
MICROBIAL PATHOGENESIS, 1997, 22 (03) :143-154