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Series GSE10165 Query DataSets for GSE10165
Status Public on Jan 05, 2009
Title Evolution of virulence control by the staphylococcal agr quorum-sensing regulator
Platform organisms Coxiella burnetii; Rickettsia rickettsii; Chlamydia muridarum; Chlamydia pneumoniae AR39; Staphylococcus epidermidis RP62A; Staphylococcus epidermidis ATCC 12228; Staphylococcus aureus subsp. aureus MW2; Borreliella burgdorferi B31; Coxiella burnetii RSA 493; Chlamydia caviae GPIC; Chlamydia trachomatis D/UW-3/CX; Staphylococcus haemolyticus JCSC1435; Granulibacter bethesdensis
Sample organism Staphylococcus aureus
Experiment type Expression profiling by array
Summary The Staphylococcus aureus accessory gene regulator (agr) is a prototype quorum-sensing system in Gram-positive bacteria and a paradigmatic example of gene regulation by a small regulatory RNA, RNAIII. Using genome-wide transcriptional profiling in the community-associated methicillin-resistant (CA-MRSA) strain MW2, we demonstrate here that in contrast to the current model of target gene regulation by agr, a large subset of agr-regulated genes is controlled independently of RNAIII. This group comprised predominantly metabolism genes, whereas virulence factors were mostly controlled by RNAIII. Remarkably, the phenol-soluble modulin (PSM) leukocidin genes were the only virulence determinants under RNAIII-independent control, emphasizing their exceptional role in S. aureus physiology and pathogenesis. Of note, PSM promoters bound the AgrA response regulator protein, previously believed to interact exclusively with agr promoters, explaining the exceptionally strict control of PSMs by agr. Our results suggest that virulence factor control is a secondary acquisition of the agr regulon, which evolved by development of RNAIII around the mRNA of the PSM d-toxin, exemplifying how gene control via a small regulatory RNA may be linked to a pre-established regulatory circuit. In addition to elucidating agr control in CA-MRSA, which revealed features potentially crucial for CA-MRSA pathogenesis, our study establishes a novel two-level model of cell-density dependent gene regulation in S. aureus and gives important insight into the connection of metabolism and virulence control in this leading opportunistic pathogen.
Keywords: Wild type control vs mutant
 
Overall design Wild type in triplicate is compared to mutant in triplicate totalling 27 samples
 
Contributor(s) Queck SY, Jameson-Lee M, Villaruz AE, Bach TL, Khan B, Sturdevant DE, Li M, Otto M
Citation(s) 18851841
Submission date Jan 14, 2008
Last update date Jul 20, 2012
Contact name Dan Sturdevant
E-mail(s) dsturdevant@niaid.nih.gov
Phone 4063639248
Organization name NIH
Department NIAID
Lab RTS
Street address 903 S 4th street
City Hamilton
State/province MT
ZIP/Postal code 59840
Country USA
 
Platforms (1)
GPL4692 [RMLchip3a520351] Affymetrix RML Custom Pathogenic chip 3
Samples (27)
GSM256988 wild type MW2 for JQ_1 series biological rep 1
GSM256989 wild type MW2 for JQ_1 series biological rep 2
GSM256990 wild type MW2 for JQ_1 series biological rep 3
Relations
BioProject PRJNA108363

Download family Format
SOFT formatted family file(s) SOFTHelp
MINiML formatted family file(s) MINiMLHelp
Series Matrix File(s) TXTHelp

Supplementary file Size Download File type/resource
GSE10165_RAW.tar 51.5 Mb (http)(custom) TAR (of CEL, CHP)
Processed data included within Sample table
Processed data provided as supplementary file
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