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Journal of Bacteriology, April 2009, p. 2012-2022, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01547-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

Mutations in ampG and Lytic Transglycosylase Genes Affect the Net Release of Peptidoglycan Monomers from Vibrio fischeri ^,

Dawn M. Adin,¹ Jacquelyn T. Engle,² William E. Goldman,^2,3 Margaret J. McFall-Ngai,⁴ and Eric V. Stabb^1*

Department of Microbiology, University of Georgia, Athens, Georgia 30605,¹ Department of Molecular Microbiology, Washington University, St. Louis, Missouri 63110,² Department of Microbiology and Immunology, University of North Carolina, Chapel Hill, North Carolina 27517,³ Department of Medical Microbiology and Immunology, University of Wisconsin, Madison, Wisconsin 53706⁴

Received 31 October 2008/ Accepted 5 December 2008

The light-organ symbiont Vibrio fischeri releases N-acetylglucosaminyl-1,6-anhydro-N-acetylmuramylalanyl--glutamyldiaminopimelylalanine, a disaccharide-tetrapeptide component of peptidoglycan that is referred to here as "PG monomer." In contrast, most gram-negative bacteria recycle PG monomer efficiently, and it does not accumulate extracellularly. PG monomer can stimulate normal light-organ morphogenesis in the host squid Euprymna scolopes, resulting in regression of ciliated appendages similar to that triggered by infection with V. fischeri. We examined whether the net release of PG monomers by V. fischeri resulted from lytic transglycosylase activity or from defects in AmpG, the permease through which PG monomers enter the cytoplasm for recycling. An ampG mutant displayed a 100-fold increase in net PG monomer release, indicating that AmpG is functional. The ampG mutation also conferred the uncharacteristic ability to induce light-organ morphogenesis even when placed in a nonmotile flaJ mutant that cannot infect the light-organ crypts. We targeted five potential lytic transglycosylase genes singly and in specific combinations to assess their role in PG monomer release. Combinations of mutations in ltgA, ltgD, and ltgY decreased net PG monomer release, and a triple mutant lacking all three of these genes had little to no accumulation of PG monomers in culture supernatants. This mutant colonized the host as well as the wild type did; however, the mutant-infected squid were more prone to later superinfection by a second V. fischeri strain. We propose that the lack of PG monomer release by this mutant results in less regression of the infection-promoting ciliated appendages, leading to this propensity for superinfection.

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* Corresponding author. Mailing address: University of Georgia, Department of Microbiology, 1000 Cedar Street, Athens, GA 30602. Phone: (706) 542-2414. Fax: (706) 542-2674. E-mail: estabb{at}uga.edu

Published ahead of print on 12 December 2008.

Supplemental material for this article may be found at http://jb.asm.org/.

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Journal of Bacteriology, April 2009, p. 2012-2022, Vol. 191, No. 7
0021-9193/09/$08.00+0     doi:10.1128/JB.01547-08
Copyright © 2009, American Society for Microbiology. All Rights Reserved.

This article has been cited by other articles:

• Nyholm, S. V. (2009). Peptidoglycan Monomer Release and Vibrio fischeri. J. Bacteriol. 191: 1997-1999 [Full Text]