Journal article

Publication year: 2005

Pages: 8385-8394

Journal: Journal of Bacteriology

Volume number: 187

Issue number: 24

ISSN: 0021-9193

eISSN: 1098-5530

Open access status: Green

DOI Link: https://doi.org/10.1128/JB.187.24.8385-8394.2005

Publisher: American Society for Microbiology

Abstract: 
We examined eight spontaneously occurring rough mutants of Listeria monocytogenes for their ability to express two previously reported autolysins, p60 and MurA. All mutants lack MurA expression and show strongly reduced levels of extracellular p60. One rough strain harbors a variant of the p60 protein with a partially truncated catalytic domain. In seven cases there were shifts in the localization of p60 to the membrane fraction. Mutations within the secA2 gene, encoding an auxiliary protein secretion system paralog, were previously shown to be involved in the smooth-rough phenotypic variation seen with Listeria strains. An isogenic Delta secA2 EGDe deletion strain displays a strong pleiotropic reduction of p60 and MurA, in addition to a large number of secreted and surface proteins. However, we observed no apparent SecA2 dysfunction in several of the investigated strains as determined by direct sequencing of the secA2 gene and complementation of the Delta secA2 mutant with the respective allele cloned from the rough mutant. To determine the gene products required for the smooth-rough transition, we created mutants lacking the individual iap and murA genes as well as a Delta iap Delta murA double mutant. The double mutant displays a rough phenotype and exhibits many of the properties seen with the Delta secA2 mutant. Our results implicate p60 and MurA as important determinants in controlling the cell shape of L. monocytogenes. We also identified homologous MurA and SecA2 proteins in other Listeria species. The muramidase in two species, L. innocua and L. welshimeri, shows activity similar to that of the MurA protein in L. monocytogenes.

Harvard Citation style: Machata, S., Hain, T., Rohde, M. and Chakraborty, T. (2005) Simultaneous deficiency of both MurA and p60 proteins generates a rough phenotype in Listeria monocytogenes, Journal of Bacteriology, 187(24), pp. 8385-8394. https://doi.org/10.1128/JB.187.24.8385-8394.2005

APA Citation style: Machata, S., Hain, T., Rohde, M., & Chakraborty, T. (2005). Simultaneous deficiency of both MurA and p60 proteins generates a rough phenotype in Listeria monocytogenes. Journal of Bacteriology. 187(24), 8385-8394. https://doi.org/10.1128/JB.187.24.8385-8394.2005