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Review

Taking control: Hijacking of Rab GTPases by intracellular bacterial pathogens

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Pages 182-191 | Received 02 Nov 2016, Accepted 25 May 2017, Published online: 05 Jul 2017

Figures & data

Figure 1. Trafficking model of the Mycobacterium-containing vacuole. After phagocytosis the Mycobacterium-containing vacuole acquires early-phagocytic features and Rab GTPases (green circles). However, it does not interact with the late endocytic pathway and does not acquire lysosomal markers, such as lysosomal hydrolases, the vATPase and lysosomal glycoproteins.

Figure 1. Trafficking model of the Mycobacterium-containing vacuole. After phagocytosis the Mycobacterium-containing vacuole acquires early-phagocytic features and Rab GTPases (green circles). However, it does not interact with the late endocytic pathway and does not acquire lysosomal markers, such as lysosomal hydrolases, the vATPase and lysosomal glycoproteins.

Table 1. Bacterial virulence factors, their biochemical activities, targets and effects on Rab GTPase function.

Figure 2. Trafficking model of the Salmonella-containing vacuole. (A) After phagocytosis the Salmonella-containing vacuole (SCV) acquires first early-endocytic features and later most of the lysosomal features. It also acquires sequentially early endocytic Rab GTPases and Rab7 (green circles). However, lysosomal hydrolases are not delivered to the SCV due to a SifA-mediated block of Rab9- and MPR-dependent transport pathway. Broad-host range Salmonella serovars, such as S. Typhimurium, target Rab32 and related Rab GTPases through GtgE and SopD2 and consequently inhibit the delivery of lysosome-related organelle (LRO) enzymes and antimicrobial factors to the LRO and SCV. (B) In contrast to the majority of other Salmonella serovars, the human-adapted S. Typhi does not deliver GtgE and SopD2 and, consequently, succumbs to the Rab32-dependent antimicrobial pathway in mice.

Figure 2. Trafficking model of the Salmonella-containing vacuole. (A) After phagocytosis the Salmonella-containing vacuole (SCV) acquires first early-endocytic features and later most of the lysosomal features. It also acquires sequentially early endocytic Rab GTPases and Rab7 (green circles). However, lysosomal hydrolases are not delivered to the SCV due to a SifA-mediated block of Rab9- and MPR-dependent transport pathway. Broad-host range Salmonella serovars, such as S. Typhimurium, target Rab32 and related Rab GTPases through GtgE and SopD2 and consequently inhibit the delivery of lysosome-related organelle (LRO) enzymes and antimicrobial factors to the LRO and SCV. (B) In contrast to the majority of other Salmonella serovars, the human-adapted S. Typhi does not deliver GtgE and SopD2 and, consequently, succumbs to the Rab32-dependent antimicrobial pathway in mice.

Figure 3. Trafficking model of the Legionella-containing vacuole. After phagocytosis the Legionella-containing vacuole (LCV) does not interact with the endocytic pathway and does not acquire any of endocytic Rab GTPases (green circles). However, it acquires the secretory Rab, Rab1, which is regulated and post-translationally modified by the Legionella T4SS effectors, DrrA, AnkX, SidD, Lem3, LepB and SidE.

Figure 3. Trafficking model of the Legionella-containing vacuole. After phagocytosis the Legionella-containing vacuole (LCV) does not interact with the endocytic pathway and does not acquire any of endocytic Rab GTPases (green circles). However, it acquires the secretory Rab, Rab1, which is regulated and post-translationally modified by the Legionella T4SS effectors, DrrA, AnkX, SidD, Lem3, LepB and SidE.

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