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Infection and Immunity, February 2007, p. 592-603, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01278-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.

The Legionella pneumophila Effector SidJ Is Required for Efficient Recruitment of Endoplasmic Reticulum Proteins to the Bacterial Phagosome{triangledown}

Yancheng Liu and Zhao-Qing Luo*

Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, Indiana 47907

Received 9 August 2006/ Returned for modification 29 September 2006/ Accepted 2 November 2006

The virulence of Legionella pneumophila is dependent on the Dot/Icm type IV protein secretion system, which translocates effectors into infected cells. A large number of such translocated proteins have been identified, but few of these proteins are necessary for intracellular replication of the pathogen, making it difficult to correlate these genes with specific cell-biological events associated with L. pneumophila infection. We report here the identification and characterization of a family of two substrates, SidJ and SdjA, with distinctive phenotypes. In contrast to many Dot/Icm substrates, whose expression levels are elevated when bacteria are grown to postexponential phase, SidJ is produced at a constant rate during the entire bacterial growth cycle. Mutation in sidJ causes a significant growth defect in both macrophage and amoeba hosts, but an sdjA mutant is detectably defective only in protozoan hosts. However, in the amoeba host a mutant lacking both sidJ and sdjA does not display a more severe growth defect than the sidJ mutant. Despite its significant intracellular growth defect, the sidJ mutant is still able to effectively evade fusion with lysosomes. Importantly, recruitment of endoplasmic reticulum (ER) proteins by vacuoles containing the sidJ mutant was considerably delayed in both mammalian and amoeba cells. Our results suggest that SidJ modulates host cellular pathways, contributing to the trafficking or retention of ER-derived vesicles to L. pneumophila vacuoles.

* Corresponding author. Mailing address: Department of Biological Sciences, Purdue University, 915 West State Street, West Lafayette, IN 47907. Phone: (765) 496-6697. Fax: (765) 494-0876. E-mail: luoz{at}purdue.edu.

{triangledown} Published ahead of print on 13 November 2006.

Editor: V. J. DiRita

Infection and Immunity, February 2007, p. 592-603, Vol. 75, No. 2
0019-9567/07/$08.00+0     doi:10.1128/IAI.01278-06
Copyright © 2007, American Society for Microbiology. All Rights Reserved.



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