The SAV1322 gene from Staphylococcus aureus: genomic and proteomic approaches to identification and characterization of gene function.
Bacterial two-component regulatory systems (TCRS) are associated with the expression of virulence factors and antibiotic susceptibility. In Staphylococcus aureus, 16 TCRS types have been identified. The histidine kinase/response regulator SAV1321/SAV1322 in the S. aureus shares considerable homology with the TCRS DesKR in Bacillus subtilis. However, a function for the SAV1322 locus has not yet been assigned.



Deletion of the SAV1322 locus in S. aureus results in reduced growth when cultured under low (25 °C) and high (46 °C) temperature conditions. The sav1322 deletion mutant is more tolerant to oxidative stress in vitro and is less pathogenic in a murine infection model when compared with wild-type parent strain Mu50. Furthermore, the sav1322 mutant exhibits lower MICs for gentimicin, tetracyclines and glycopeptides, increased autolysis, and a thinner cell wall when compared with the wild-type strain. Microarray and proteomic analyses show that the expression of cell-wall-associated genes glmS and murZ are lower, and the expression of heat shock and stress-related genes (hrcA, ctsR, dnaK, dnaJ, grpE, clpB, and clpC) are higher in the sav1322 mutant when compared with the wild-type strain. In addition, the sav1322 mutant displays altered expression of proteins involved in carbohydrate/energy metabolism, cell wall metabolism, and stress or heat shock response, as well as other metabolic processes including lipid metabolism, amino acid biosynthesis, purine or pyrimidine metabolism, transcription, and protein biosynthesis.



The S. aureus SAV1322 locus plays a pronounced role in temperature adaptation, antibiotic resistance, and virulence by regulating a wide range of genes and proteins involved in metabolism and stress tolerance.
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Jung Wook
JW
Kim
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Hyun-Kyung
HK
Kim
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Gi Su
GS
Kang
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Il-Hwan
IH
Kim
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Hwa Su
HS
Kim
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea.
Yeong Seon
YS
Lee
Division of Antimicrobial Resistance, Center for Infectious Diseases, National Research Institute of Health, Centers for Disease Control and Prevention, Cheongju, South Korea. knihyoo@naver.com.|Korea National Research Institute of Health, Osong Health Technology Administration Complex, 187, Osongsaengmyeong2-ro, Osong-eup, Heungdeok-gu, Cheongju-si, Chungcheongbuk-do, 363-700, South Korea. knihyoo@naver.com.
Jae Il
JI
Yoo
D000818:Animals; D001426:Bacterial Proteins / Q000235:genetics; D001483:Base Sequence; D002473:Cell Wall / Q000378:metabolism; D004195:Disease Models, Animal; D024881:Drug Resistance, Bacterial / Q000235:genetics; D004352:Drug Resistance, Microbial / Q000235:genetics; D005260:Female; D017353:Gene Deletion; D015964:Gene Expression Regulation, Bacterial / Q000502:physiology*; D055786:Gene Knockout Techniques; D005798:Genes, Bacterial / Q000187:drug effects / Q000502:physiology*; D040342:Genetic Structures / Q000235:genetics* / Q000502:physiology*; D023281:Genomics; D006360:Heat-Shock Proteins / Q000235:genetics; D000071677:Histidine Kinase / Q000494:pharmacology; D051379:Mice; D008807:Mice, Inbred BALB C; D046529:Microscopy, Electron, Transmission; D051189:Murinae; D018384:Oxidative Stress; D010641:Phenotype; D040901:Proteomics; D013203:Staphylococcal Infections / Q000382:microbiology; D013211:Staphylococcus aureus / Q000166:cytology / Q000235:genetics* / Q000254:growth & development / Q000378:metabolism; D013315:Stress, Psychological / Q000235:genetics; D013696:Temperature; D037521:Virulence Factors / Q000235:genetics
D001426:Bacterial Proteins; D006360:Heat-Shock Proteins; D037521:Virulence Factors; D000071677:Histidine Kinase
Heat shock proteins; Microarray analysis; Microbial drug resistance; Physiological stress; Proteomics; Staphylococcus aureus