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Chapter 8 : Cell Biology of the Chlamydial Inclusion

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Cell Biology of the Chlamydial Inclusion, Page 1 of 2

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Abstract:

All aspects of survival are intimately linked to the cell biology of its host. Recent advances in cell biological techniques and new tools to perform loss-of-function experiments in mammalian cells have accelerated one's understanding of the extent to which manipulates the host. Homotypic fusion of inclusions could serve to consolidate resources and reduce competition among multiple growing inclusions. It is clear that Incs on early inclusions likely play important roles in remodeling the nascent inclusion to segregate from the endolysosomal pathway and maintain single inclusion morphology in fusogenic species. However, the role played by soluble effectors secreted early or even during entry should not be discounted when considering early interactions with host cell biology. Of host sphingolipids (SLs), only sphingomyelin, and not glucosylceramide, is delivered to the chlamydial inclusion , suggesting highly specific interactions with host pathways. Multivesicular bodies (MVBs) are late endocytic compartments in which the limiting membrane of endosomes has invaginated into the lumen to form intraluminal vesicles containing membrane proteins destined for degradation. Much of the focus of investigations into chlamydial anti-immune strategies has centered on the interruption of innate immune signaling pathways. Given the long evolutionary history of the association of spp. with eukaryotic cells, these bacteria are expected to reveal new insights into basic aspects of eukaryotic cell biology, primordial mechanisms of cell autonomous innate immunity, and novel pathogenic strategies.

Citation: Kokes M, Valdivia R. 2012. Cell Biology of the Chlamydial Inclusion, p 170-191. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch8
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FIGURE 1

Early events in nascent inclusion biogenesis. Soon after chlamydial entry, the nascent inclusion rapidly loses plasma membrane and early endocytic and classic endolysosomal markers ( ), including the phosphoinositides PI(4,5)P and PI3P and endolysosomal Rabs (Rab5, Rab7, and Rab9) ( ). Recycling endosomes and their associated Rabs localize to early inclusions ( ) and may facilitate migration to the MTOC, in a microtubule- and dynein-dependent manner ( ). p150, the component of the dynactin protein complex linking vesicular cargo to dynein, is required for migration to the MTOC, although p50 dynamitin is not ( ). inclusion membrane proteins IncB and Ct850 are postulated to play a role in this interaction to promote association of the nascent inclusion with the microtubule-organizing center ( ). Endocytic pathway-associated SNAREs, including Vamp3, -7, and -8, localize around the inclusion in a fusion-inhibited state potentially as a result of interactions with Incs (IncA, CT813, and CT223) ( ). These Inc proteins have been proposed to function as inhibitory SNARE (iSNARE) mimics ( ). doi:10.1128/9781555817329.ch8.f1

Citation: Kokes M, Valdivia R. 2012. Cell Biology of the Chlamydial Inclusion, p 170-191. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch8
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Image of FIGURE 2
FIGURE 2

The inclusion interacts with multiple subcellular compartments. Fragmented Golgi apparatus ministacks, the ER, LDs, mitochondria, and recycling endosomes (RE) closely associate with the inclusion ( ). These interactions may facilitate nutrient acquisition directly from these organelles. Golgi apparatus fragmentation enhances sphingolipid uptake ( ), and lipid droplets translocate into the lumen of the inclusion ( ). Additional pathways for lipid delivery (inset) include vesicular transport of Golgi apparatus-derived exocytic vesicles ( ), MVBs ( ), and transfer at membrane contact sites (MCS) between the ER and inclusion membranes ( ). The inclusion remains in close association with centrosomes at the MTOC throughout intracellular infection ( ). doi:10.1128/9781555817329.ch8.f2

Citation: Kokes M, Valdivia R. 2012. Cell Biology of the Chlamydial Inclusion, p 170-191. In Tan M, Bavoil P (ed), Intracellular Pathogens I: . ASM Press, Washington, DC. doi: 10.1128/9781555817329.ch8
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