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Infect Immun, May 1998, p. 1934-1940, Vol. 66, No. 5
Department of Microbiology and Immunology,
College of Medicine, Chandler Medical Center, University of Kentucky,
Lexington, Kentucky 40536-0084,1 and
School of Biological Sciences, University of
Kentucky, Lexington, Kentucky 40506-02252
Received 13 October 1997/Returned for modification 18 November
1997/Accepted 12 February 1998
Cytolethal distending toxin (CDT) from the diarrheagenic bacterium
Campylobacter jejuni was shown to cause a rapid and
specific cell cycle arrest in HeLa and Caco-2 cells. Within 24 h
of treatment, CDT caused HeLa cells to arrest with a 4N DNA
content, indicative of cells in G2 or early M phase.
Immunofluorescence studies indicated that the arrested cells had not
entered M phase, since no evidence of tubulin reorganization or
chromatin condensation was visible. CDT treatment was also shown to
cause HeLa cells to accumulate the inactive, tyrosine-phosphorylated
form of CDC2. These results indicated that CDT treatment results in a
failure to activate CDC2, which leads to cell cycle arrest in
G2. This mechanism of action is novel for a bacterial toxin
and provides a model for the generation of diarrheal disease by
C. jejuni and other diarrheagenic bacteria that produce
CDT.
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.
Campylobacter jejuni Cytolethal
Distending Toxin Causes a G2-Phase Cell Cycle
Block

*
Corresponding author. Mailing address: Department of
Microbiology and Immunology, Chandler Medical Center, 800 Rose St.,
University of Kentucky, Lexington, KY 40536-0084. Phone: (606)
323-5313. Fax: (606) 257-8994. E-mail:
cpicket{at}pop.uky.edu.
Present address: Department of Microbiology and Immunology,
University of Rochester, School of Medicine and Dentistry, Rochester, NY 14642.
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