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Host -adducin is redistributed and localized to the inclusion membrane in Chlamydia- and Chlamydophila-infected cells

Hencelyn G. Chu^1,2,

¹ Department of Biomedical Sciences, College of Veterinary Medicine, Oregon State University, Corvallis, OR 97331-4804, USA
² Department of Microbiology, Oregon State University, Corvallis, OR 97331-3804, USA
³ Puget Sound Blood Center, University of Washington, Seattle, WA 98104, USA

Correspondence
Daniel D. Rockey
rockeyd{at}orst.edu

A large-scale analysis of proteins involved in host-cell signalling pathways was performed using chlamydia-infected murine cells in order to identify host proteins that are differentially activated or localized following infection. Two proteins whose distribution was altered in Chlamydia trachomatis-infected cells relative to mock-infected cells were the actin-binding protein adducin and the regulatory kinase Raf-1. Immunoblot analysis with antibodies to both phosphorylated and non-phosphorylated forms of these proteins demonstrated that the abundance of each protein was markedly reduced in the cytosolic fraction of C. trachomatis- and Chlamydophila caviae-infected cells, but the total cellular protein abundance remained unaffected by infection. Fluorescence microscopy of chlamydia-infected cells using anti--adducin antibodies demonstrated labelling at or near the chlamydial inclusion membrane. Treatment of infected cells with nocodazole or cytochalasin D did not affect -adducin that was localized to the margins of the inclusion. The demonstration of -adducin and Raf-1 redistribution within cells infected by different chlamydiae provides novel opportunities for analysis of host–pathogen interactions in this system.

Present address: Department of Pathology and Laboratory Medicine, University of California, Irvine, CA 92697-4800, USA.

A supplementary table comparing the abundance of phosphorylated proteins in infected vs mock-infected samples or lysates is available with the online version of this paper.