CoChat
Sign Up
Cited by 14

The DOI matches its Crossref record; 1 of the 1 references it cites were found in a registry or an index.

Systematic study of genes influencing cellular chain length in Streptococcus sanguinis

Evans, Karra, Stone, Victoria, Chen, Lei, Ge, Xiuchun, Xu, Ping·2014·Microbiology
DOI 10.1099/mic.0.071688-0PMC PMC3919539
Open this paper in CoChat — free account

Abstract

Streptococcus sanguinis is a Gram-positive bacterium that is indigenous to the oral cavity. S. sanguinis, a primary colonizer of the oral cavity, serves as a tether for the attachment of other oral pathogens. The colonization of microbes on the tooth surface forms dental plaque, which can lead to the onset of periodontal disease. We examined a comprehensive mutant library to identify genes related to cellular chain length and morphology using phase-contrast microscopy. A number of hypothetical genes related to the cellular chain length were identified in this study. Genes related to the cellular chain length were analysed along with clusters of orthologous groups (COG) for gene functions. It was discovered that the highest proportion of COG functions related to cellular chain length was ‘cell division and chromosome separation’. However, different COG functions were also found to be related with altered cellular chain length. This suggested that different genes related with multiple mechanisms contribute to the cellular chain length in S. sanguinis SK36.

Overview

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Integrity signals

Registry

Crossref · 10.1099/mic.0.071688-0

Cites

1 of 1 references verified0 citation errors · 0 not checkable

Statistics

Figures

Fig. 1. Chain morphologies of mutants. (a) SK36, the wild-type strain. (b) A longer chain mutant with deletion of SSA_0933 gene for acetyltransferase. (c) A shorter chain mutant with deletion of SSA_0422 gene for phosphoglycerate mutase family protein. (d) A chain clustered mutant with deletion of SSA_0285 gene for formate acetyltransferase 3.
Fig. 1. Chain morphologies of mutants. (a) SK36, the wild-type strain. (b) A longer chain mutant with deletion of SSA_0933 gene for acetyltransferase. (c) A shorter chain mutant with deletion of SSA_0422 gene for phosphoglycerate mutase family protein. (d) A chain clustered mutant with deletion of SSA_0285 gene for formate acetyltransferase 3.CC BY · PubMed Central
Fig. 2. Cellular chain length and auto-aggregation of selected mutants and their complementation. Upper panel, the cellular chain lengths of mutants and their complemented strains were examined and compared with the wild-type (WT) as described in Methods. Lower panel, their auto-aggregations were determined by OD600 and the aggregation percentage was calculated as described in Methods. * P<0.05. Error bars indicate ±sd.
Fig. 2. Cellular chain length and auto-aggregation of selected mutants and their complementation. Upper panel, the cellular chain lengths of mutants and their complemented strains were examined and compared with the wild-type (WT) as described in Methods. Lower panel, their auto-aggregations were determined by OD600 and the aggregation percentage was calculated as described in Methods. * P<0.05. Error bars indicate ±sd.CC BY · PubMed Central
Fig. 3. Cellular chain length related gene distribution by COG functions. The ratio between the number of longer chain or shorter chain mutants and the total number of annotated genes in the genome (gene percentage) was calculated for every COG function. COG function abbreviations: Q, secondary metabolites biosynthesis, transport and catabolism; P, inorganic ion transport and metabolism; D, cell division and chromosome partitioning; T, signal transduction mechanisms; E, amino acid transport and metabolism; H, coenzyme metabolism; M, cell envelope biogenesis, outer membrane; G, carbohydrate transport and metabolism; L, DNA replication, recombination and repair; K, transcription; O, post-translational modification, protein turnover, chaperones; C, energy production and conversion; R, general function prediction only; S, function unknown; N, cell motility and secretion; F, nucleotide transport and metabolism; I, lipid metabolism; J, translation, ribosomal structure and biogenesis.
Fig. 3. Cellular chain length related gene distribution by COG functions. The ratio between the number of longer chain or shorter chain mutants and the total number of annotated genes in the genome (gene percentage) was calculated for every COG function. COG function abbreviations: Q, secondary metabolites biosynthesis, transport and catabolism; P, inorganic ion transport and metabolism; D, cell division and chromosome partitioning; T, signal transduction mechanisms; E, amino acid transport and metabolism; H, coenzyme metabolism; M, cell envelope biogenesis, outer membrane; G, carbohydrate transport and metabolism; L, DNA replication, recombination and repair; K, transcription; O, post-translational modification, protein turnover, chaperones; C, energy production and conversion; R, general function prediction only; S, function unknown; N, cell motility and secretion; F, nucleotide transport and metabolism; I, lipid metabolism; J, translation, ribosomal structure and biogenesis.CC BY · PubMed Central
Fig. 4. Cell morphological comparisons by SEM. (a) The wild-type strain SK36. (b) Ssx_0655, a cell division protein FtsA mutant, shows wider and longer cells. (c) Ssx_2223, a capsular polysaccharide biosynthesis protein Wzd (chain length regulator) mutant, shows clear capsule surrounding the cells. Septum (S), Z-ring (Z) and polysaccharide (P) are indicated. Bars, 1 μm.
Fig. 4. Cell morphological comparisons by SEM. (a) The wild-type strain SK36. (b) Ssx_0655, a cell division protein FtsA mutant, shows wider and longer cells. (c) Ssx_2223, a capsular polysaccharide biosynthesis protein Wzd (chain length regulator) mutant, shows clear capsule surrounding the cells. Septum (S), Z-ring (Z) and polysaccharide (P) are indicated. Bars, 1 μm.CC BY · PubMed Central

Verification

Claims the paper makes

The claims and statistics of this paper haven’t been checked yet.

Run the check — free, no account needed. It reads the open-access text and checks the sources it cites.

A few free checks a day · papers already verified open instantly · results are public

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Self-check

Percentages, sums and reported differences re-computed from the paper’s own numbers.

The self-check needs the paper’s full text.

Citations

Cites

Research works printed but not linked: 26

  1. Ahmed, 2003, Viridans streptococcus bacteremia in children on chemotherapy for cancer: an underestimated problem, Pediatr Hematol Oncol, 20, 439, 10.1080/08880010390220144 · DOI
  2. 10.1111/j.1365-2672.2010.04935.x · DOI
  3. 10.1099/mic.0.039669-0 · DOI
  4. 10.1016/j.chom.2011.09.009 · DOI
  5. 10.1111/j.1365-2958.2011.07828.x · DOI
  6. Higgins, 1970, Site of initiation of cellular autolysis in Streptococcus faecalis as seen by electron microscopy, J Bacteriol, 103, 504, 10.1128/JB.103.2.504-512.1970 · DOI
  7. 10.1128/JB.187.18.6536-6544.2005 · DOI
  8. Kilian, 1981, Ecology and nature of immunoglobulin A1 protease-producing streptococci in the human oral cavity and pharynx, Infect Immun, 31, 868, 10.1128/IAI.31.3.868-873.1981 · DOI
  9. 10.1099/00207713-39-4-471 · DOI
  10. Kolenbrander, 1993, Adhere today, here tomorrow: oral bacterial adherence, J Bacteriol, 175, 3247, 10.1128/JB.175.11.3247-3252.1993 · DOI
  11. 10.1111/j.1365-2958.2004.04432.x · DOI
  12. 10.1016/j.micpath.2008.05.009 · DOI
  13. Murchison, 1982, Isolation and characterization of Streptococcus mutans mutants with altered cellular morphology or chain length, Infect Immun, 38, 282, 10.1128/IAI.38.1.282-291.1982 · DOI
  14. 10.1016/j.micinf.2005.04.012 · DOI
  15. 10.1099/mic.0.26363-0 · DOI
  16. 10.1111/j.1600-0765.1977.tb00112.x · DOI
  17. 10.1038/emboj.2012.76 · DOI · Paper page
  18. 10.1093/nar/29.1.22 · DOI
  19. 10.1111/j.1399-302X.1991.tb00500.x · DOI
  20. 10.1099/00207713-47-3-908 · DOI
  21. 10.1128/IAI.00760-09 · DOI
  22. Wang, 1990, High-level expression of the FtsA protein inhibits cell septation in Escherichia coli K-12, J Bacteriol, 172, 4736, 10.1128/JB.172.8.4736-4740.1990 · DOI
  23. 10.1128/AEM.68.3.1196-1203.2002 · DOI
  24. 10.1128/JB.01808-06 · DOI
  25. 10.1038/srep00125 · DOI
  26. 10.1111/j.1574-6976.2007.00098.x · DOI

Cited by

Sorted by citations

See all 14

Metadata

Authors
Evans, K., Stone, V., Chen, L., Ge, X., & Xu, P.
Venue
Microbiology
Publisher
Microbiology Society
Published
2014-02-01
Volume
160
Issue
2
Pages
307-315
ISSN
  • 1350-0872
  • 1465-2080
DOI
10.1099/mic.0.071688-0
PMC
PMC3919539
Cited by
14
References
1
Language
en
Funders
  • Incentive Program (144602-3)
  • Virginia Commonwealth University Presidential Research
  • National Institutes of Health (R01DE018138, R01DE023078)

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review