دورية أكاديمية
Staphylococcus aureus aconitase inactivation unexpectedly inhibits post-exponential-phase growth and enhances stationary-phase survival.
| العنوان: | Staphylococcus aureus aconitase inactivation unexpectedly inhibits post-exponential-phase growth and enhances stationary-phase survival. |
|---|---|
| المؤلفون: | Somerville GA; Laboratory of Human Bacterial Pathogenesis. Rocky Mountain Microscopy Branch. Rocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Hamilton, Montana 59840, USA., Chaussee MS, Morgan CI, Fitzgerald JR, Dorward DW, Reitzer LJ, Musser JM |
| المصدر: | Infection and immunity [Infect Immun] 2002 Nov; Vol. 70 (11), pp. 6373-82. |
| نوع المنشور: | Journal Article |
| اللغة: | English |
| بيانات الدورية: | Publisher: American Society For Microbiology Country of Publication: United States NLM ID: 0246127 Publication Model: Print Cited Medium: Print ISSN: 0019-9567 (Print) Linking ISSN: 00199567 NLM ISO Abbreviation: Infect Immun Subsets: MEDLINE |
| أسماء مطبوعة: | Publication: Washington, DC : American Society For Microbiology Original Publication: [Bethesda, Md.] American Society for Microbiology. |
| مواضيع طبية MeSH: | Aconitate Hydratase/*physiology , Staphylococcus aureus/*enzymology , Staphylococcus aureus/*growth & development, Acetates/metabolism ; Amino Acids/metabolism ; Animals ; Bacterial Proteins/genetics ; Citric Acid Cycle ; Glucose/metabolism ; Mice ; Mice, Hairless ; Proteome ; Sigma Factor/genetics ; Staphylococcus aureus/pathogenicity ; Trans-Activators/genetics ; Virulence |
| مستخلص: | Staphylococcus aureus preferentially catabolizes glucose, generating pyruvate, which is subsequently oxidized to acetate under aerobic growth conditions. Catabolite repression of the tricarboxylic acid (TCA) cycle results in the accumulation of acetate. TCA cycle derepression coincides with exit from the exponential growth phase, the onset of acetate catabolism, and the maximal expression of secreted virulence factors. These data suggest that carbon and energy for post-exponential-phase growth and virulence factor production are derived from the catabolism of acetate mediated by the TCA cycle. To test this hypothesis, the aconitase gene was genetically inactivated in a human isolate of S. aureus, and the effects on physiology, morphology, virulence factor production, virulence for mice, and stationary-phase survival were examined. TCA cycle inactivation prevented the post-exponential growth phase catabolism of acetate, resulting in premature entry into the stationary phase. This phenotype was accompanied by a significant reduction in the production of several virulence factors and alteration in host-pathogen interaction. Unexpectedly, aconitase inactivation enhanced stationary-phase survival relative to the wild-type strain. Aconitase is an iron-sulfur cluster-containing enzyme that is highly susceptible to oxidative inactivation. We speculate that reversible loss of the iron-sulfur cluster in wild-type organisms is a survival strategy used to circumvent oxidative stress induced during host-pathogen interactions. Taken together, these data demonstrate the importance of the TCA cycle in the life cycle of this medically important pathogen. |
| References: | Appl Microbiol. 1967 Jul;15(4):866-70. (PMID: 6049306) J Ultrastruct Res. 1984 Feb;86(2):107-18. (PMID: 6539826) Am J Med. 2000 Jul;109(1):33-44. (PMID: 10936476) J Bacteriol. 2002 Mar;184(5):1430-7. (PMID: 11844774) J Bacteriol. 1999 Nov;181(22):7131-5. (PMID: 10559181) J Bacteriol. 1997 Oct;179(20):6355-9. (PMID: 9335283) Mol Microbiol. 1998 Oct;30(2):393-404. (PMID: 9791183) Infect Immun. 2001 Feb;69(2):822-31. (PMID: 11159974) J Bacteriol. 2001 May;183(10):3193-203. (PMID: 11325949) J Bacteriol. 1997 Dec;179(23):7351-9. (PMID: 9393699) Arch Biochem Biophys. 1955 Nov;59(1):260-8. (PMID: 13269177) J Biol Chem. 1992 May 5;267(13):8757-63. (PMID: 1315737) J Gen Microbiol. 1963 Nov;33:213-29. (PMID: 14121198) Proc Natl Acad Sci U S A. 1999 Aug 31;96(18):10412-7. (PMID: 10468622) Mol Microbiol. 1998 Mar;27(5):967-76. (PMID: 9535086) FEMS Microbiol Lett. 1992 Jul 1;73(1-2):133-8. (PMID: 1521761) J Mol Biol. 1975 Nov 5;98(3):503-17. (PMID: 1195397) Methods Enzymol. 1991;204:587-636. (PMID: 1658572) J Gen Microbiol. 1962 Sep;29:157-64. (PMID: 13896903) Infect Immun. 1999 Mar;67(3):1331-7. (PMID: 10024579) J Biol Chem. 1983 Sep 25;258(18):11098-105. (PMID: 6309829) Mol Microbiol. 1996 Sep;21(6):1227-37. (PMID: 8898391) Microbiology. 2002 Apr;148(Pt 4):1027-37. (PMID: 11932448) Biochem J. 1937 Apr;31(4):661-71. (PMID: 16746383) Infect Immun. 1999 Apr;67(4):1779-88. (PMID: 10085018) J Appl Microbiol. 2000 Jun;88(6):1028-37. (PMID: 10849179) Mol Microbiol. 1997 Oct;26(2):399-407. (PMID: 9383163) FEMS Microbiol Lett. 1997 Jun 1;151(1):1-8. (PMID: 9198277) Proc Natl Acad Sci U S A. 1991 Nov 15;88(22):10109-13. (PMID: 1946430) Proc Natl Acad Sci U S A. 2002 Apr 2;99(7):4662-7. (PMID: 11880608) J Gen Microbiol. 1962 Nov;29:531-5. (PMID: 14022366) Mol Microbiol. 1998 Dec;30(5):991-1001. (PMID: 9988476) J Biol Chem. 1951 Nov;193(1):265-75. (PMID: 14907713) Mol Microbiol. 1995 Sep;17(6):1143-52. (PMID: 8594333) J Biol Chem. 1967 Sep 10;242(17):3833-8. (PMID: 6037548) Microbiology. 1999 Nov;145 ( Pt 11):3069-79. (PMID: 10589714) Arch Biochem Biophys. 1953 Sep;46(1):154-63. (PMID: 13092955) |
| المشرفين على المادة: | 0 (Acetates) 0 (Amino Acids) 0 (Bacterial Proteins) 0 (Proteome) 0 (SarA protein, bacterial) 0 (SigB protein, Bacteria) 0 (Sigma Factor) 0 (Trans-Activators) EC 4.2.1.3 (Aconitate Hydratase) IY9XDZ35W2 (Glucose) |
| تواريخ الأحداث: | Date Created: 20021016 Date Completed: 20021108 Latest Revision: 20210526 |
| رمز التحديث: | 20221213 |
| مُعرف محوري في PubMed: | PMC130419 |
| DOI: | 10.1128/IAI.70.11.6373-6382.2002 |
| PMID: | 12379717 |
| قاعدة البيانات: | MEDLINE |
| تدمد: | 0019-9567 |
|---|---|
| DOI: | 10.1128/IAI.70.11.6373-6382.2002 |