Seeking completeness in bacterial mutant hunts

2006 ◽  
Vol 9 (3) ◽  
pp. 307-311 ◽  
Author(s):  
Nina R Salama ◽  
Colin Manoil
Keyword(s):  
2020 ◽  
Vol 6 (1) ◽  
pp. 87-102
Author(s):  
Emily C. Pierce ◽  
Manon Morin ◽  
Jessica C. Little ◽  
Roland B. Liu ◽  
Joanna Tannous ◽  
...  

Nature ◽  
1960 ◽  
Vol 187 (4739) ◽  
pp. 802-804 ◽  
Author(s):  
STANLEY G. SCHULTZ ◽  
A. K. SOLOMON

2003 ◽  
Vol 71 (6) ◽  
pp. 3578-3586 ◽  
Author(s):  
Jonathan M. Solomon ◽  
Grace S. Leung ◽  
Ralph R. Isberg

ABSTRACT Mycobacterium marinum causes tuberculosis-like disease in fish and amphibians and has been used as a model mycobacterial species because of its rapid growth and less stringent containment requirements relative to other mycobacterial species. We demonstrate here that M. marinum grows within Dictyostelium discoideum cells, allowing the genetic analysis of host factors that may modulate the replication of mycobacterial species. Intracellular growth of M. marinum was shown to mimic the properties previously observed for growth within cultured phagocytes. A defined bacterial mutant defective for growth within phagocytic cells was shown to be similarly defective for growth within D. discoideum. To test the role of host coronin, which was previously hypothesized to positively modulate mycobacterial growth within mouse macrophages, a defined D. discoideum coronin mutant was analyzed. Surprisingly, the absence of coronin resulted in enhanced intracellular replication of M. marinum relative to the control wild-type strain. Consistent with previous observations, some phagosomes showed persistence of coronin about the surface of the compartment, but colocalization of the protein was far from uniform. We conclude that in D. discoideum factors other than coronin support intracellular replication of M. marinum.


1982 ◽  
Vol 152 (1) ◽  
pp. 338-344
Author(s):  
J S Wolfson ◽  
D C Hooper ◽  
M N Swartz ◽  
G L McHugh

The constructed plasmid pBR322 and the native plasmid pMG110 were eliminated (cured) from growing Escherichia coli cells by the antagonism of the B subunit of the bacterial enzyme DNA gyrase. The antagonism may be by the growth of cells (i) at semipermissive temperatures in a bacterial mutant containing a thermolabile gyrase B subunit or (ii) at semipermissive concentrations of coumermycin A1, an antibiotic that specifically inhibits the B subunit of DNA gyrase. The kinetics of plasmid elimination indicate that plasmid loss occurs too rapidly to be explained solely by the faster growth of that plasmid-free bacteria and, therefore, represents interference with plasmid maintenance.


1972 ◽  
Vol 6 (12) ◽  
pp. 1577-1584 ◽  
Author(s):  
P.T.S. Wong ◽  
D. Liu ◽  
B.J. Dutka
Keyword(s):  

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