Evidence map›Paper›PMID 16549661›Full record

ArticleMicrobiology (Reading, England)2006

Defects in ex vivo and in vivo growth and sensitivity to osmotic stress of group A Streptococcus caused by interruption of response regulator gene vicR.

Mengyao Liu, Tracey S Hanks, Jinlian Zhang, Michael J McClure, Daniel W Siemsen, Julie L Elser, Mark T Quinn, Benfang Lei

Abstract read
In one paragraph

Article in Microbiology (Reading, England), 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 57 papers.

0numbers the graph read from it
0cells of the map it votes in
57citing papers in PubMed
5.1field-weighted citation impact, top 5% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

57 citing papers in PubMed, 87 citations in OpenAlex.

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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

8 authors at 1 institution in 1 country.

Mengyao LiuDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Tracey S HanksDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Jinlian ZhangDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Michael J McClureDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Daniel W SiemsenDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Julie L ElserDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Mark T QuinnDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Benfang LeiDepartment of Veterinary Molecular Biology, Montana State University, Bozeman, MT 59717, USA.
Montana State University · US

Funding

MT INBRE RESEARCH COREP20RR016455 · NCRR · MONTANA STATE UNIVERSITY - BOZEMAN · PI HARMSEN, ALLEN G · 2001 to 2011
$34.4M
VIRUSES: FROM PARTICLES TO PROTEOMICSP20RR020185 · NCRR · MONTANA STATE UNIVERSITY - BOZEMAN · PI MEISSNER, NICOLE · 2004 to 2011
$17.0M
MOLECULAR STRUCTURE OF THE PHAGOCYTE NADPH OXIDASER01AR042426 · NIAMS · MONTANA STATE UNIVERSITY - BOZEMAN · PI QUINN, MARK T · 1996 to 2007
$1.8M
Heme Acquisition in Group A StreptococcusK22AI057347 · NIAID · MONTANA STATE UNIVERSITY (BOZEMAN) · PI LEI, BENFANG · 2004 to 2005
$270k
NCRR NIH HHS P20 RR016455NCRR NIH HHS P20 RR-020185NCRR NIH HHS P20 RR020185NCRR NIH HHS P20 RR-16455NIAID NIH HHS K22 AI057347NIAMS NIH HHS AR42426NIAMS NIH HHS R01 AR042426
6 · The paper itself

Abstract

The regulator VicR of the two-component regulatory system VicRK is essential in several Gram-positive bacteria. However, the authors were able to generate an unconditional vicR insertional mutant of group A Streptococcus. This mutant grew well in rich media but not in non-immune human blood and serum, had attenuated virulence, and was unstable in mice. Complementation of the mutant with vicR expressed in trans restored its phenotype to wild-type. A vicK deletion mutant had a phenotype similar to that of the vicR mutant. Phagocytosis and killing of the vicR mutant were normal, suggesting that VicRK does not regulate processes involved in evasion of host defence. Microarray analysis showed that vicR inactivation down-regulated the transcription of 13 genes, including putative cell wall hydrolase gene pcsB and spy1058-1060, which encode a putative phosphotransferase system enzyme II for carbohydrate transport, and upregulated the expression of five genes, including spy0183 and spy0184, which encode an osmoprotectant transporter OpuA. Consistent with microarray analysis, the vicR mutant took up more of the osmoprotectants betaine and proline and was sensitive to osmotic stress, indicating that vicR inactivation induced osmotic stress and increased susceptibility to osmotic pressure. Additionally, a spy1060 deletion mutant also displayed attenuated virulence. These results suggest that VicRK regulates processes involved in cell wall metabolism, nutrient uptake, and osmotic protection.

Indexed as

Gene Expression Regulation, BacterialMutagenesis, InsertionalOsmotic PressureAnimalsBacterial ProteinsBiological TransportBloodCell WallCulture MediaDisease Models, AnimalFemaleGene DeletionGene Expression ProfilingGenes, BacterialGenetic Complementation TestHumansBacterial ProteinsCulture MediaYycF protein, Bacteria

Identifiers

PMID16549661
PMCPMC2423276
OpenAlexW2129234138

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.