1887

Chapter 12 : The Scr Circuit in Modulates Swarming and Sticking

Author: Linda L. McCarter1
VIEW AFFILIATIONS HIDE AFFILIATIONS
Affiliations: 1: Department of Microbiology, The University of Iowa, Iowa City, IA 52242
Content Type: Monograph
Publication Year: 2010

Category: Microbial Genetics and Molecular Biology

MyBook is a cheap paperback edition of the original book and will be sold at uniform, low price.

Preview this chapter:
Preview Magnify
Zoom in
Zoomout

The Scr Circuit in Modulates Swarming and Sticking, Page 1 of 2

| /docserver/preview/fulltext/10.1128/9781555816667/9781555814991_Chap12-1.gif /docserver/preview/fulltext/10.1128/9781555816667/9781555814991_Chap12-2.gif

Abstract:

The role of c-di-GMP in determining the switch between motile and sessile lifestyles appears to be an emerging theme in many bacteria; in some bacteria, one important consequence is an impact on virulence. Scr (swarming and capsular polysaccharide gene regulation) genes influence the lifestyle adaptation between swarming and sticking by modulating the cellular nucleotide pool. Fractionation experiments localize ScrA to the cytoplasm, ScrB in the periplasm, and ScrC with the cell membrane. Curiously, overproduction of ScrC without coproduction of ScrA and ScrB does not simply result in loss of increased expression but rather recapitulates the ScrABC phenotype. In contrast, both the GGDEF and the EAL domains of ScrC possess catalytic activity: by itself (in the absence of ScrA and ScrB), ScrC can synthesize c-di-GMP (in as well as in ), whereas in the context of functional ScrA and ScrB, ScrC is capable of degrading this secondary messenger. In comparison, the activity of ScrC seems to be modulated by ScrA and ScrB. The enzymes controlling the level of c-di-GMP include proteins with GGDEF and EAL domains as well as the phosphohydrolase-associated HD-GYP domain. In possessing a multiplicity of cell types appropriate for life under different circumstances, the swimmer, swarmer, and sticky cell types, the ubiquitous marine bacterium and human pathogen must make certain critical lifestyle determinations. c-di-GMP plays a key role by influencing this decision-making process.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Highlighted Text: Show | Hide
Loading full text...

Full text loading...

Figures

The Scr Circuit in Vibrio parahaemolyticus Modulates Swarming and Sticking
[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555816667.ch12-1,webId=/content/author/10.1128/9781555816667.ch12-1,properties={foaf_givenname=Linda L., foaf_name=Linda L. McCarter, foaf_surname=McCarter, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555816667.ch12-aff1]]}]]
Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
/content/10.1128/9781555816667.ch12.ch12fig01
Figure 1.
Lifestyle decision for to swim, swarm, or stick? When growing in liquid, the highly motile swimmer cell is propelled by a single polar flagellum. Upon contact with surfaces, this polar flagellum is no longer an effective propulsive organelle. Unable to rotate its polar flagellum, the organism must decide whether to induce a second flagellar system and differentiate to the elongated, hyperflagellated swarmer cell or to orchestrate the production of sticky cell surface molecules promoting adhesion and biofilm development. This decision is modulated by Scr sensors that are thought to integrate environmental information by modulating the level of c-di-GMP. High levels of c-di-GMP promote the sessile lifestyle, whereas low levels of c-di-GMP enhance surface motility.
10.1128/9781555816667/f0174-01_thmb.gif
10.1128/9781555816667/f0174-01.gif
Image of Figure 1.
Figure 1.

Lifestyle decision for to swim, swarm, or stick? When growing in liquid, the highly motile swimmer cell is propelled by a single polar flagellum. Upon contact with surfaces, this polar flagellum is no longer an effective propulsive organelle. Unable to rotate its polar flagellum, the organism must decide whether to induce a second flagellar system and differentiate to the elongated, hyperflagellated swarmer cell or to orchestrate the production of sticky cell surface molecules promoting adhesion and biofilm development. This decision is modulated by Scr sensors that are thought to integrate environmental information by modulating the level of c-di-GMP. High levels of c-di-GMP promote the sessile lifestyle, whereas low levels of c-di-GMP enhance surface motility.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint
/content/10.1128/9781555816667.ch12.ch12fig02
Figure 2.
Swarming and sticking are reciprocally influenced at the level of transcription by the operon. Mutants with defects in the operon fail to swarm on solid surfaces (A) and produce crinkly colonies on Congo red medium (B). The inability of these mutants to swarm is not the simple consequence of being too sticky to move, as they also fail to swarm upon introduction of a lesion in the CPS biosynthetic locus (C). The altered phenotypes are a consequence of altered lateral flagellar () and gene expression. Transcription was measured in (D) and (E) reporter strains.
10.1128/9781555816667/f0174-02_thmb.gif
10.1128/9781555816667/f0174-02.gif
Image of Figure 2.
Figure 2.

Swarming and sticking are reciprocally influenced at the level of transcription by the operon. Mutants with defects in the operon fail to swarm on solid surfaces (A) and produce crinkly colonies on Congo red medium (B). The inability of these mutants to swarm is not the simple consequence of being too sticky to move, as they also fail to swarm upon introduction of a lesion in the CPS biosynthetic locus (C). The altered phenotypes are a consequence of altered lateral flagellar () and gene expression. Transcription was measured in (D) and (E) reporter strains.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint
/content/10.1128/9781555816667.ch12.ch12fig03
Figure 3.
ScrC is a bifunctional enzyme whose activity is influenced by ScrA and ScrB. (A) Examination of P-labeled nucleotides extracted from a Δ strain carrying expression clones by using two-dimensional thin-layer chromatography (2D-TLC). The small arrows indicate control spots to provide orientation, and the large arrow indicates c-di-GMP. ScrABC decreases the c-di-GMP spot, the EAL domain is critical for the phosphodiesterase (PDE) activity of ScrABC, and ScrC produced by itself (without the context of functional ScrA and ScrB) increases the level of this nucleotide. (B) The EAL domain determines the PDE activity of ScrABC but not the diguanylate cyclase activity of ScrC: phenotypes of the wild-type (Wt) strain on swarm plates and Congo red medium upon ectopic expression of alleles.
10.1128/9781555816667/f0175-01_thmb.gif
10.1128/9781555816667/f0175-01.gif
Image of Figure 3.
Figure 3.

ScrC is a bifunctional enzyme whose activity is influenced by ScrA and ScrB. (A) Examination of P-labeled nucleotides extracted from a Δ strain carrying expression clones by using two-dimensional thin-layer chromatography (2D-TLC). The small arrows indicate control spots to provide orientation, and the large arrow indicates c-di-GMP. ScrABC decreases the c-di-GMP spot, the EAL domain is critical for the phosphodiesterase (PDE) activity of ScrABC, and ScrC produced by itself (without the context of functional ScrA and ScrB) increases the level of this nucleotide. (B) The EAL domain determines the PDE activity of ScrABC but not the diguanylate cyclase activity of ScrC: phenotypes of the wild-type (Wt) strain on swarm plates and Congo red medium upon ectopic expression of alleles.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint
/content/10.1128/9781555816667.ch12.ch12fig04
Figure 4.
ScrG is a second GGDEF-EAL protein participating in the control of swarming and sticking. (A) Although the phenotype is less profound than the phenotype on standard swarming agar, defects become apparent on low-salt swarming medium, which is less permissive for swarming than the standard high-salt swarming medium. The phenotype can be complemented by or but not by . (B) The effects of and are cumulative on swarming and colony morphology but not on swimming. Wild-type and mutant strains were inoculated in high-salt swarm plates (1.5% agar), high-salt, iron-supplemented (enhances colony rugosity) swarm plates (1.5% agar), Congo red medium (2% agar), and semisolid swim medium (0.3% agar). ScrG mutants (row 4) show slight impairment of swarming on high-salt agar; however, in combination with an deletion, the ability of the double mutant (row 3) to swarm is more defective than that of the single mutant strain (row 2). In addition, the colony morphology of the double mutant strain is more crinkly than either of the single mutant strains (shown on high-iron and Congo red media). The system has a negligible impact on swimming motility: all mutants show little difference in their ability to swim compared to the wild type.
10.1128/9781555816667/f0177-01_thmb.gif
10.1128/9781555816667/f0177-01.gif
Image of Figure 4.
Figure 4.

ScrG is a second GGDEF-EAL protein participating in the control of swarming and sticking. (A) Although the phenotype is less profound than the phenotype on standard swarming agar, defects become apparent on low-salt swarming medium, which is less permissive for swarming than the standard high-salt swarming medium. The phenotype can be complemented by or but not by . (B) The effects of and are cumulative on swarming and colony morphology but not on swimming. Wild-type and mutant strains were inoculated in high-salt swarm plates (1.5% agar), high-salt, iron-supplemented (enhances colony rugosity) swarm plates (1.5% agar), Congo red medium (2% agar), and semisolid swim medium (0.3% agar). ScrG mutants (row 4) show slight impairment of swarming on high-salt agar; however, in combination with an deletion, the ability of the double mutant (row 3) to swarm is more defective than that of the single mutant strain (row 2). In addition, the colony morphology of the double mutant strain is more crinkly than either of the single mutant strains (shown on high-iron and Congo red media). The system has a negligible impact on swimming motility: all mutants show little difference in their ability to swim compared to the wild type.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint
/content/10.1128/9781555816667.ch12.ch12fig05
Figure 5.
Model of the Scr c-di-GMP circuit in transcriptional control of swarming and sticking. Two GGDEF-EAL proteins, ScrC and ScrG, regulate swarming and sticking gene expression by acting as phosphodiesterases to modulate the level of c-di-GMP. The phosphodiesterase activity of ScrC is controlled by interaction with ScrA, a predicted pyridoxal phosphate-dependent aminotransferase, and ScrB, a predicted periplasmic solute-binding protein. Potentially, input signals transmitted via the periplasmic sensing domain of ScrC and the PAS domain of ScrG may moderate the activity of the output GGDEF-EAL domains. High levels of c-di-GMP promote production of CPS production and biofilm formation, and low levels of this signaling molecule promote swarming motility. Additional output targets include a predicted cell surface adhesin binding chitin or -acetylglucosamine (VPA1598) and the operon, which encodes a type I membrane fusion transport system that is known to play a role in biofilm development (VPA1443-5). The nature of the input signals and how alterations in the cellular c-di-GMP pool affect transcription of lateral flagellar and genes are not known, although Cps-specific transcriptional regulators (CpsR and CpsS) participating in this circuit have been identified. This model also predicts the existence of additional GGDEF-, EAL-, or HD-GYP-type Scr sensors, and current work is focused on identifying new members of the Scr sensory array.
10.1128/9781555816667/f0178-01_thmb.gif
10.1128/9781555816667/f0178-01.gif
Image of Figure 5.
Figure 5.

Model of the Scr c-di-GMP circuit in transcriptional control of swarming and sticking. Two GGDEF-EAL proteins, ScrC and ScrG, regulate swarming and sticking gene expression by acting as phosphodiesterases to modulate the level of c-di-GMP. The phosphodiesterase activity of ScrC is controlled by interaction with ScrA, a predicted pyridoxal phosphate-dependent aminotransferase, and ScrB, a predicted periplasmic solute-binding protein. Potentially, input signals transmitted via the periplasmic sensing domain of ScrC and the PAS domain of ScrG may moderate the activity of the output GGDEF-EAL domains. High levels of c-di-GMP promote production of CPS production and biofilm formation, and low levels of this signaling molecule promote swarming motility. Additional output targets include a predicted cell surface adhesin binding chitin or -acetylglucosamine (VPA1598) and the operon, which encodes a type I membrane fusion transport system that is known to play a role in biofilm development (VPA1443-5). The nature of the input signals and how alterations in the cellular c-di-GMP pool affect transcription of lateral flagellar and genes are not known, although Cps-specific transcriptional regulators (CpsR and CpsS) participating in this circuit have been identified. This model also predicts the existence of additional GGDEF-, EAL-, or HD-GYP-type Scr sensors, and current work is focused on identifying new members of the Scr sensory array.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint
/content/10.1128/9781555816667.ch12.ch12fig06
Figure 6.
Additional output targets of the Scr circuit. c-di-GMP affects transcription of two known additional targets. Colonies containing bioluminescence () fusions were grown overnight on plates and photographed in the dark. All colonies grew equally well on the plate, but only the luminous colonies appear in the photograph. The luminescence of is enhanced by low levels of c-di-GMP (the consequence of overexpression of ) and repressed by high levels of c-di-GMP (upon overexpression of ) compared to strains carrying a vector control. In contrast, the fusion in is regulated oppositely, i.e., light production is enhanced by high levels of c-di-GMP and repressed by low levels of the nucleotide signal. Both genes encode predicted cell surface moieties. VPA1598 encodes a chitin- or -acetylglucosamine-binding protein. VPA1443 is in the operon, which encodes an RTX transporter system known to participate in biofilm development and affect colony morphology. Thus the Scr circuit, originally named for swarming and cps regulation, influences warming and ell surface egulation.
10.1128/9781555816667/f0182-01_thmb.gif
10.1128/9781555816667/f0182-01.gif
Image of Figure 6.
Figure 6.

Additional output targets of the Scr circuit. c-di-GMP affects transcription of two known additional targets. Colonies containing bioluminescence () fusions were grown overnight on plates and photographed in the dark. All colonies grew equally well on the plate, but only the luminous colonies appear in the photograph. The luminescence of is enhanced by low levels of c-di-GMP (the consequence of overexpression of ) and repressed by high levels of c-di-GMP (upon overexpression of ) compared to strains carrying a vector control. In contrast, the fusion in is regulated oppositely, i.e., light production is enhanced by high levels of c-di-GMP and repressed by low levels of the nucleotide signal. Both genes encode predicted cell surface moieties. VPA1598 encodes a chitin- or -acetylglucosamine-binding protein. VPA1443 is in the operon, which encodes an RTX transporter system known to participate in biofilm development and affect colony morphology. Thus the Scr circuit, originally named for swarming and cps regulation, influences warming and ell surface egulation.

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
Permissions and Reprints Request Permissions
Download as Powerpoint

References

/content/book/10.1128/9781555816667.ch12
1. Andrade, M. O.,, M. C. Alegria,, C. R. Guzzo,, C. Docena,, M. C. Rosa,, C. H. Ramos, and, C. S. Farah. 2006. The HD-GYP domain of RpfG mediates a direct linkage between the Rpf quorum-sensing pathway and a subset of diguanylate cyclase proteins in the phytopathogen Xanthomonas axonopodis pv citri. Mol. Microbiol. 62: 537– 551.
2. Benach, J.,, S. S. Swaminathan,, R. Tamayo,, S. K. Handelman,, E. Folta-Stogniew,, J. E. Ramos,, F. Forouhar,, H. Neely,, J. Seetharaman,, A. Camilli, and, J. F. Hunt. 2007. The structural basis of cyclic diguanylate signal transduction by PilZ domains. EMBO J. 26: 5153– 5166.
3. Beyhan, S.,, K. Bilecen,, S. R. Salama,, C. Casper-Lindley, and, F. H. Yildiz. 2007. Regulation of rugosity and biofilm formation in Vibrio cholerae: comparison of VpsT and VpsR regulons and epistasis analysis of vpsT, vpsR, and hapR. J. Bacteriol. 189: 388– 402.
4. Beyhan, S.,, A. D. Tischler,, A. Camilli, and, F. H. Yildiz. 2006. Transcriptome and phenotypic responses of Vibrio cholerae to increased cyclic di-GMP level. J. Bacteriol. 188: 3600– 3613.
5. Bobrov, A. G.,, O. Kirillina, and, R. D. Perry. 2005. The phosphodiesterase activity of the HmsP EAL domain is required for negative regulation of biofilm formation in Yersinia pestis. FEMS Microbiol. Lett. 247: 123– 130.
6. Boles, B. R., and, L. L. McCarter. 2002. Vibrio parahaemolyticus scrABC, a novel operon affecting swarming and capsular polysaccharide regulation. J. Bacteriol. 184: 5946– 5954.
7. Bomchil, N.,, P. Watnick, and, R. Kolter. 2003. Identification and characterization of a Vibrio cholerae gene, mbaA, involved in maintenance of biofilm architecture. J. Bacteriol. 185: 1384– 1390.
8. Casper-Lindley,, C., and, F. H. Yildiz. 2004. VpsT is a transcriptional regulator required for expression of vps biosynthesis genes and the development of rugose colonial morphology in Vibrio cholerae O1 El Tor. J. Bacteriol. 186: 1574– 1578.
9. Chan, C.,, R. Paul,, D. Samoray,, N. C. Amiot,, B. Giese,, U. Jenal, and, T. Schirmer. 2004. Structural basis of activity and allosteric control of diguanylate cyclase. Proc. Natl. Acad. Sci. USA 101: 17084– 17089.
10. Christen, M.,, B. Christen,, M. G. Allan,, M. Folcher,, P. Jeno,, S. Grzesiek, and, U. Jenal. 2007. DgrA is a member of a new family of cyclic diguanosine monophosphate receptors and controls flagellar motor function in Caulobacter crescentus. Proc. Natl. Acad. Sci. USA 104: 4112– 4117.
11. Cotter, P. A., and, S. Stibitz. 2007. c-di-GMP-mediated regulation of virulence and biofilm formation. Curr. Opin. Microbiol. 10: 17– 23.
12. D’Argenio,, D. A.,, M. W. Calfee,, P. B. Rainey, and, E. C. Pesci. 2002. Autolysis and autoaggregation in Pseudomonas aeruginosa colony morphology mutants. J. Bacteriol. 184: 6481– 6489.
13. Darnell, C. L.,, E. A. Hussa, and, K. L. Visick. 2008. The putative hybrid sensor kinase SypF coordinates biofilm formation in Vibrio fischeri by acting upstream of two response regulators, SypG and VpsR. J. Bacteriol. 190: 4941– 4950.
14. Dow, J. M.,, Y. Fouhy,, J. F. Lucey, and, R. P. Ryan. 2006. The HD-GYP domain, cyclic di-GMP signaling, and bacterial virulence to plants. Mol. Plant-Microbe Interact. 19: 1378– 1384.
15. Enos-Berlage,, J. L.,, Z. T. Guvener,, C. E. Keenan, and, L. L. McCarter. 2005. Genetic determinants of biofilm development of opaque and translucent Vibrio parahaemolyticus. Mol. Microbiol. 55: 1160– 1182.
16. Ferreira, R. B.,, L. C. Antunes,, E. P. Greenberg, and, L. L. McCarter. 2008. Vibrio parahaemolyticus ScrC modulates cyclic dimeric GMP regulation of gene expression relevant to growth on surfaces. J. Bacteriol. 190: 851– 860.
17. Galperin, M. Y. 2004. Bacterial signal transduction network in a genomic perspective. Environ. Microbiol. 6: 552– 567.
18. Galperin, M. Y., and, A. N. Nikolskaya. 2007. Identification of sensory and signal-transducing domains in two-component signaling systems. Methods Enzymol. 422: 47– 74.
19. Guvener, Z. T., and, L. L. McCarter. 2003. Multiple regulators control capsular polysaccharide production in Vibrio parahaemolyticus. J. Bacteriol. 185: 5431– 5441.
20. Hickman, J. W., and, C. S. Harwood. 2008. Identification of FleQ from Pseudomonas aeruginosa as a c-di-GMP-responsive transcription factor. Mol. Microbiol. 69: 376– 389.
21. Hickman, J. W.,, D. F. Tifrea, and, C. S. Harwood. 2005. A chemosensory system that regulates biofilm formation through modulation of cyclic diguanylate levels. Proc. Natl. Acad. Sci. USA 102: 14422– 14427.
22. Huang, B.,, C. B. Whitchurch, and, J. S. Mattick. 2003. FimX, a multidomain protein connecting environmental signals to twitching motility in Pseudomonas aeruginosa. J. Bacteriol. 185: 7068– 7076.
23. Inoue, T.,, R. Shingaki,, S. Hirose,, K. Waki,, H. Mori, and, K. Fukui. 2007. Genome-wide screening of genes required for swarming motility in Escherichia coli K-12. J. Bacteriol. 189: 950– 957.
24. Jenal, U., and, J. Malone. 2006. Mechanisms of cyclic-di-GMP signaling in bacteria. Annu. Rev. Genet. 40: 385– 407.
25. Karatan, E.,, T. R. Duncan, and, P. I. Watnick. 2005. NspS, a predicted polyamine sensor, mediates activation of Vibrio cholerae biofilm formation by norspermidine. J. Bacteriol. 187: 7434– 7443.
26. Kawagishi, I.,, M. Imagawa,, Y. Imae,, L. McCarter, and, M. Homma. 1996. The sodium-driven polar flagellar motor of marine Vibrio as the mechanosensor that regulates lateral flagellar expression. Mol. Microbiol. 20: 693– 699.
27. Kim, Y. K., and, L. L. McCarter. 2007. ScrG, a GGDEF-EAL protein, participates in regulating swarming and sticking in Vibrio parahaemolyticus. J. Bacteriol. 189: 4094– 4107.
28. Kirillina, O.,, J. D. Fetherston,, A. G. Bobrov,, J. Abney, and, R. D. Perry. 2004. HmsP, a putative phosphodiesterase, and HmsT, a putative diguanylate cyclase, control Hms-dependent biofilm formation in Yersinia pestis. Mol. Microbiol. 54: 75– 88.
29. Kuchma, S. L.,, K. M. Brothers,, J. H. Merritt,, N. T. Liberati,, F. M. Ausubel, and, G. A. O’Toole. 2007. BifA, a cyclic-di-GMP phosphodiesterase, inversely regulates biofilm formation and swarming motility by Pseudomonas aeruginosa PA14. J. Bacteriol. 189: 8165– 8178.
30. Lee, V. T.,, J. M. Matewish,, J. L. Kessler,, M. Hyodo,, Y. Hayakawa, and, S. Lory. 2007. A cyclic-di-GMP receptor required for bacterial exopolysaccharide production. Mol. Microbiol. 65: 1474– 1484.
31. Lim, B.,, S. Beyhan,, J. Meir, and, F. H. Yildiz. 2006. Cyclic-diGMP signal transduction systems in Vibrio cholerae: modulation of rugosity and biofilm formation. Mol. Microbiol. 60: 331– 348.
32. Mayer, R.,, P. Ross,, H. Weinhouse,, D. Amikam,, G. Volman,, P. Ohana,, R. D. Calhoon,, H. C. Wong,, A. W. Emerick, and, M. Benziman. 1991. Polypeptide composition of bacterial cyclic diguanylic acid-dependent cellulose synthase and the occurrence of immunologically crossreacting proteins in higher plants. Proc. Natl. Acad. Sci. USA 88: 5472– 5476.
33. McCarter, L.,, M. Hilmen, and, M. Silverman. 1988. Flagellar dynamometer controls swarmer cell differentiation of V. parahaemolyticus. Cell 54: 345– 351.
34. Merighi, M.,, V. T. Lee,, M. Hyodo,, Y. Hayakawa, and, S. Lory. 2007. The second messenger bis-(3′-5′)-cyclic-GMP and its PilZ domain-containing receptor Alg44 are required for alginate biosynthesis in Pseudomonas aeruginosa. Mol. Microbiol. 65: 876– 895.
35. Merritt, J. H.,, K. M. Brothers,, S. L. Kuchma, and, G. A. O’Toole. 2007. SadC reciprocally influences biofilm formation and swarming motility via modulation of exopolysaccharide production and flagellar function. J. Bacteriol. 189: 8154– 8164.
36. Overhage, J.,, S. Lewenza,, A. K. Marr, and, R. E. Hancock. 2007. Identification of genes involved in swarming motility using a Pseudomonas aeruginosa PAO1 mini-Tn5-lux mutant library. J. Bacteriol. 189: 2164– 2169.
37. Paul, R.,, S. Weiser,, N. C. Amiot,, C. Chan,, T. Schirmer,, B. Giese, and, U. Jenal. 2004. Cell cycle-dependent dynamic localization of a bacterial response regulator with a novel diguanylate cyclase output domain. Genes Dev. 18: 715– 727.
38. Pesavento, C.,, G. Becker,, N. Sommerfeldt,, A. Possling,, N. Tschowri,, A. Mehlis, and, R. Hengge. 2008. Inverse regulatory coordination of motility and curli-mediated adhesion in Escherichia coli. Genes Dev. 22: 2434– 2446.
39. Pratt, J. T.,, R. Tamayo,, A. D. Tischler, and, A. Camilli. 2007. PilZ domain proteins bind cyclic diguanylate and regulate diverse processes in Vibrio cholerae. J. Biol. Chem. 282: 12860– 12870.
40. Rashid, M. H.,, C. Rajanna,, A. Ali, and, D. K. Karaolis. 2003. Identification of genes involved in the switch between the smooth and rugose phenotypes of Vibrio cholerae. FEMS Microbiol. Lett. 227: 113– 119.
41. Rather, P. N. 2005. Swarmer cell differentiation in Proteus mirabilis. Environ. Microbiol. 7: 1065– 1073.
42. Romling, U. 2005. Characterization of the rdar morphotype, a multicellular behaviour in Enterobacteriaceae. Cell. Mol. Life Sci. 62: 1234– 1246.
43. Romling, U., and, D. Amikam. 2006. Cyclic di-GMP as a second messenger. Curr. Opin. Microbiol. 9: 218– 228.
44. Ryan, R. P.,, Y. Fouhy,, J. F. Lucey, and, J. M. Dow. 2006. Cyclic di-GMP signaling in bacteria: recent advances and new puzzles. J. Bacteriol. 188: 8327– 8334.
45. Ryjenkov, D. A.,, R. Simm,, U. Römling, and, M. Gomelsky. 2006. The PilZ domain is a receptor for the second messenger c-di-GMP: the PilZ domain protein YcgR controls motility in enterobacteria. J. Biol. Chem. 281: 30310– 30314.
46. Schmidt, A. J.,, D. A. Ryjenkov, and, M. Gomelsky. 2005. The ubiquitous protein domain EAL is a cyclic diguanylate-specific phosphodiesterase: enzymatically active and inactive EAL domains. J. Bacteriol. 187: 4774– 4781.
47. Simm, R.,, M. Morr,, A. Kader,, M. Nimtz, and, U. Römling. 2004. GGDEF and EAL domains inversely regulate cyclic di-GMP levels and transition from sessility to motility. Mol. Microbiol. 53: 1123– 1134.
48. Stewart, B. J. 2002. Investigating Surface-Induced Gene Expression: the Lateral Flagellar Gene System of Vibrio parahaemolyticus. Ph.D. dissertation. The University of Iowa, Iowa City.
49. Sudarsan, N.,, E. R. Lee,, Z. Weinberg,, R. H. Moy,, J. N. Kim,, K. H. Link, and, R. R. Breaker. 2008. Riboswitches in eubacteria sense the second messenger cyclic di-GMP. Science 321: 411– 413.
50. Tamayo, R.,, J. T. Pratt, and, A. Camilli. 2007. Roles of cyclic diguanylate in the regulation of bacterial pathogenesis. Annu. Rev. Microbiol. 61: 131– 148.
51. Tarutina, M.,, D. A. Ryjenkov, and, M. Gomelsky. 2006. An unorthodox bacteriophytochrome from Rhodobacter sphaeroides involved in turnover of the second messenger c-di-GMP. J. Biol. Chem. 281: 34751– 34758.
52. Tischler, A. D., and, A. Camilli. 2004. Cyclic diguanylate (c-di-GMP) regulates Vibrio cholerae biofilm formation. Mol. Microbiol. 53: 857– 869.
53. Waters, C. M.,, W. Lu,, J. D. Rabinowitz, and, B. L. Bassler. 2008. Quorum sensing controls biofilm formation in Vibrio cholerae through modulation of cyclic di-GMP levels and repression of vpsT. J. Bacteriol. 190: 2527– 2536.
54. Weinhouse, H.,, S. Sapir,, D. Amikam,, Y. Shilo,, G. Volman,, P. Ohana, and, M. Benziman. 1997. c-di-GMP-binding protein, a new factor regulating cellulose synthesis in Acetobacter xylinum. FEBS Lett. 416: 207– 211.
55. Wolfe, A. J., and, K. L. Visick. 2008. Get the message out: cyclic-di-GMP regulates multiple levels of flagellum-based motility. J. Bacteriol. 190: 463– 475.
56. Yildiz, F. H.,, N. A. Dolganov, and, G. K. Schoolnik. 2001. VpsR, a member of the response regulators of the two-component regulatory systems, is required for expression of vps biosynthesis genes and EPS ETr-associated phenotypes in Vibrio cholerae O1 El Tor. J. Bacteriol. 183: 1716– 1726.

Tables

The Scr Circuit in Vibrio parahaemolyticus Modulates Swarming and Sticking
[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/author/10.1128/9781555816667.ch12-1,webId=/content/author/10.1128/9781555816667.ch12-1,properties={foaf_givenname=Linda L., foaf_name=Linda L. McCarter, foaf_surname=McCarter, pub_isAffiliatedWith=[com.pub2web.rdf.cci.facet.ContentItem[id=http://asm.metastore.ingenta.com/content/affiliation/10.1128/9781555816667.ch12-aff1]]}]]
Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12
/content/10.1128/9781555816667.ch12.ch12tab01
Table 1
V. proteins with GGDEF, EAL, or HD domains
Generic image for table
Table 1

V. proteins with GGDEF, EAL, or HD domains

Citation: McCarter L. 2010. The Scr Circuit in Modulates Swarming and Sticking, p 173-185. In Wolfe A, Visick K (ed), The Second Messenger Cyclic Di-GMP. ASM Press, Washington, DC. doi: 10.1128/9781555816667.ch12

Back to top
This is a required field
Please enter a valid email address
Please check the format of the address you have entered.
Approval was a Success
Invalid data
An Error Occurred
Approval was partially successful, following selected items could not be processed due to error