The combination of energy-dependent internal adaptation mechanisms and external factors enables Listeria monocytogenes to express a strong starvation survival response during multiple-nutrient starvation.
The goal of this study was to characterize the starvation survival response (SSR) of a wild-type Listeria monocytogenes 10403S and an isogenic DeltasigB mutant strain during multiple-nutrient starvation conditions over 28 days. This study examined the effects of inhibitors of protein synthesis, the proton motive force, substrate level phosphorylation, and oxidative phosphorylation on the SSR of L. monocytogenes 10403S and a DeltasigB mutant during multiple-nutrient starvation. The effects of starvation buffer changes on viability were also examined. During multiple-nutrient starvation, both strains expressed a strong SSR, suggesting that L. monocytogenes possesses SigB-independent mechanism(s) for survival during multiple-nutrient starvation. Neither strain was able to express an SSR following starvation buffer changes, indicating that the nutrients/factors present in the starvation buffer could be a source of energy for cell maintenance and survival. Neither the wild-type nor the DeltasigB mutant strain was able to elicit an SSR when exposed to the protein synthesis inhibitor chloramphenicol within the first 4 h of starvation. However, both strains expressed an SSR when exposed to chloramphenicol after 6 h or more of starvation, suggesting that the majority of proteins required to elicit an effective SSR in L. monocytogenes are likely produced somewhere between 4 and 6 h of starvation. The varying SSRs of both strains to the different metabolic inhibitors under aerobic or anaerobic conditions suggested that (1) energy derived from the proton motive force is important for an effective SSR, (2) L. monocytogenes utilizes an anaerobic electron transport during multiple-nutrient starvation conditions, and (3) the glycolytic pathway is an important energy source during multiple-nutrient starvation when oxygen is available, and less important under anaerobic conditions. Collectively, the data suggest that the combination of energy-dependent internal adaptation mechanisms of cells and external nutrients/factors enables L. monocytogenes to express a strong SSR.
Lungu
Bwalya
B
Department of Food Science, Institute for Food Science and Engineering, University of Arkansas, Fayetteville, Arkansas 72704, USA.
Saldivar
Joshua C
JC
Story
Robert
R
Ricke
Steven C
SC
Johnson
Michael G
MG
D000222:Adaptation, Physiological / Q000187:drug effects / Q000235:genetics; D000332:Aerobiosis / Q000187:drug effects / Q000235:genetics; D000693:Anaerobiosis / Q000187:drug effects / Q000235:genetics; D015169:Colony Count, Microbial; D004579:Electron Transport / Q000187:drug effects; D004734:Energy Metabolism / Q000187:drug effects / Q000235:genetics; D004791:Enzyme Inhibitors / Q000494:pharmacology; D005517:Foodborne Diseases / Q000517:prevention & control; D006019:Glycolysis / Q000502:physiology; D008089:Listeria monocytogenes / Q000235:genetics / Q000254:growth & development / Q000502:physiology*; D050296:Microbial Viability / Q000187:drug effects / Q000235:genetics; D010085:Oxidative Phosphorylation / Q000187:drug effects; D010766:Phosphorylation / Q000187:drug effects; D014176:Protein Biosynthesis / Q000187:drug effects; D011500:Protein Synthesis Inhibitors / Q000494:pharmacology; D018892:Proton-Motive Force / Q000187:drug effects; D012808:Sigma Factor / Q000235:genetics / Q000502:physiology; D013312:Stress, Physiological / Q000187:drug effects / Q000235:genetics; D013997:Time Factors; D014475:Uncoupling Agents / Q000494:pharmacology
D004791:Enzyme Inhibitors; D011500:Protein Synthesis Inhibitors; C480945:SigB protein, Listeria monocytogenes; D012808:Sigma Factor; D014475:Uncoupling Agents