Possible role of inositol phospholipid signal transduction system inDunaliella salina under hypoosmotic shock

1997 ◽  
Vol 42 (2) ◽  
pp. 151-155
Author(s):  
Sixue Chen ◽  
Lin Li ◽  
Jiqiong Yan ◽  
Zhengkai Xu ◽  
Xinzhi Jiao
Keyword(s):  
Signal Transduction ◽  
Signal Transduction System ◽  
Hypoosmotic Shock ◽  
Inositol Phospholipid

scholarly journals The LisRK Signal Transduction System Determines the Sensitivity of Listeria monocytogenes to Nisin and Cephalosporins

2002 ◽  
Vol 46 (9) ◽  
pp. 2784-2790 ◽  
Author(s):  
Paul D. Cotter ◽  
Caitriona M. Guinane ◽  
Colin Hill
Keyword(s):  
Signal Transduction ◽  
Listeria Monocytogenes ◽  
Histidine Kinase ◽  
Antimicrobial Agents ◽  
Response Regulator ◽  
Signal Transduction System ◽  
Enhanced Sensitivity ◽  
Virulence Potential ◽  
Two Component Signal Transduction

ABSTRACT The Listeria monocytogenes two-component signal transduction system, LisRK, initially identified in strain LO28, plays a significant role in the virulence potential of this important food-borne pathogen. Here, it is shown that, in addition to its major contribution in responding to ethanol, pH, and hydrogen peroxide stresses, LisRK is involved in the ability of the cell to tolerate important antimicrobials used in food and in medicine, e.g., the lantibiotic nisin and the cephalosporin family of antibiotics. A ΔlisK mutant (lacking the LisK histidine kinase sensor component) displays significantly enhanced resistance to the lantibiotic nisin, a greatly enhanced sensitivity to the cephalosporins, and a large reduction in the expression of three genes thought to encode a penicillin-binding protein, another histidine kinase (other than LisK), and a protein of unknown function. Confirmation of the role of LisRK was obtained when the response regulator, LisR, was overexpressed using both constitutive and inducible (nisin-controlled expression) systems. Under these conditions we observed a reversion of the ΔlisK mutant to wild-type growth kinetics in the presence of nisin. It was also found that overexpression of LisR complemented the reduced expression of two of the aforementioned genes. These results demonstrate the important role of LisRK in the response of L. monocytogenes to a number of antimicrobial agents.

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