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| Status |
Public on May 16, 2024 |
| Title |
Catabolite control protein C (CcpC) contributes to virulence and hydrogen peroxide-induced oxidative stress responses in Listeria monocytogenes |
| Organism |
Listeria monocytogenes serotype 4b str. F2365 |
| Experiment type |
Expression profiling by high throughput sequencing
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| Summary |
Listeria monocytogenes causes listeriosis, an infectious and potentially fatal disease of animals and humans. A diverse network of transcriptional regulators, including LysR-type catabolite control protein C (CcpC), is critical for the survival of L. monocytogenes and its ability to transition into the host environment. In this study, we explored the physiological and genetic consequences of deleting ccpC and the effects of such deletion on the ability of L. monocytogenes to cause disease. We found that ccpC deletion did not impact hemolytic activity, whereas it resulted in significant reductions in phospholipase activities. Western blotting revealed that the ΔccpC strain produced significantly reduced levels of the cholesterol-dependent cytolysin LLO relative to the wildtype F2365 strain. However, the ΔccpC mutant displayed no significant intracellular growth defect in macrophages. Furthermore, ΔccpC strain exhibited reduction in plaque numbers in fibroblasts compared to F2365, but plaque size was not significantly affected by ccpC deletion. In a murine model system, the ΔccpC strain exhibited a significantly reduced bacterial burden in the liver and spleen compared to the wildtype F2365 strain. Interestingly, the deletion of this gene also enhanced the survival of L. monocytogenes under conditions of H2O2-induced oxidative stress. Transcriptomic analyses performed under H2O2-induced oxidative stress conditions revealed that DNA repair, cellular responses to DNA damage and stress, metalloregulatory proteins, and genes involved in the biosynthesis of peptidoglycan and teichoic acids were significantly induced in the ccpC deletion strain relative to F2365. In contrast, genes encoding internalin, 1-phosphatidylinositol phosphodiesterase, and genes associated with sugar-specific phosphotransferase system components, porphyrin, branched-chain amino acids, and pentose phosphate pathway were significantly downregulated in the ccpC deletion strain relative to F2365. This finding highlights CcpC as a key factor that regulates L. monocytogenes physiology and responses to oxidative stress by controlling the expression of important metabolic pathways.
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| Overall design |
To further investigate the mechanism underlying the reduced susceptibility of the ΔccpC strain to oxidative stress conditions, we examined the regulatory role of CcpC following exposure to H2O2-induced oxidative stress. RNA-seq was performed on total RNA harvested from wildtype and ΔccpC cultures that had been grown to exponential phase and then exposed to 8 mM H2O2 for 2.5
d1031 is the ccpC mutant strain while d1759 is a gltC mutant strain
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| Contributor(s) |
Ogunleye SC, Islam S, Kader Chowdhury QM, Ozdemir O, Lawrence ML, Abdelhamed H |
| Citation missing |
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| Submission date |
May 16, 2024 |
| Last update date |
May 16, 2024 |
| Contact name |
Hossam Abdelhamed |
| E-mail(s) |
abdelhamed@cvm.msstate.edu
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| Organization name |
CVM
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| Street address |
Wise drive
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| City |
Mississippi State |
| ZIP/Postal code |
39762 |
| Country |
USA |
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| Platforms (1) |
| GPL34483 |
Illumina NovaSeq 6000 (Listeria monocytogenes serotype 4b str. F2365) |
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| Samples (9)
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| Relations |
| BioProject |
PRJNA1112372 |
| Supplementary file |
Size |
Download |
File type/resource |
| GSE267669_FPKM.txt.gz |
163.8 Kb |
(ftp)(http) |
TXT |
| GSE267669_d1031vsWT_deg_all.txt.gz |
157.5 Kb |
(ftp)(http) |
TXT |
| GSE267669_d1759vsWT_deg_all.txt.gz |
38.7 Kb |
(ftp)(http) |
TXT |
SRA Run Selector |
| Raw data are available in SRA |
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