The Obligate Intracellular Pathogen Chlamydia trachomatis Targets Host Lipid Droplets
2006; Elsevier BV; Volume: 16; Issue: 16 Linguagem: Inglês
10.1016/j.cub.2006.06.060
ISSN1879-0445
AutoresYadunanda Kumar, Jordan L. Cocchiaro, Raphael H. Valdivia,
Tópico(s)Plant Reproductive Biology
ResumoLipid droplets (LDs) are ubiquitous but poorly understood neutral-lipid-rich eukaryotic organelles that may participate in functions as diverse as lipid homeostasis, membrane traffic, and signaling [1Martin S. Parton R.G. Lipid droplets: A unified view of a dynamic organelle.Nat. Rev. Mol. Cell Biol. 2006; 7: 373-378Crossref PubMed Scopus (817) Google Scholar]. We report that infection with the obligate intracellular pathogen Chlamydia trachomatis, the causative agent of trachoma and many sexually transmitted diseases [2Schachter J. Infection and disease epidemiology.in: Stephens R.S. Chlamydia: Intracellular Biology, Pathogenesis and Immunity. A.S.M, Washington, D.C.1999: 139-169Crossref Google Scholar], leads to the accumulation of neutral-lipid-rich structures with features of LDs at the cytoplasmic surface of the bacteria-containing vacuole. To identify bacterial factors that target these organelles, we screened a collection of yeast strains expressing GFP-tagged chlamydial ORFs and identified several proteins with tropism for eukaryotic LDs. We determined that three of these LD-associated (Lda) proteins are translocated into the mammalian host and associate with neutral-lipid-rich structures. Furthermore, the stability of one Lda protein is dependent on binding to LDs, and pharmacological inhibition of LD formation negatively impacted chlamydial replication. These results suggest that C. trachomatis targets LDs to enhance its survival and replication in infected cells. The co-option of mammalian LD function by a pathogenic bacterium represents a novel mechanism of eukaryotic organelle subversion and provides unique research opportunities to explore the function of these understudied organelles.
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