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Frontiers in infectious diseases > 11. Bacterial exploitation of host cytoskeleton and intracellular trafficking > Flashcards

11. Bacterial exploitation of host cytoskeleton and intracellular trafficking Flashcards

1
Q

What has allowed pathogens to be able to manipulate host cells?

A

Intimate involvement between pathogens and host

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2
Q

What cellular processes can bacteria exploit?

A
  1. Cytoskeleton dynamics
  2. Membrane trafficking
  3. Phosphoinisitol lipid metabolism
  4. Post-translational modification
  5. Apoptosis
  6. Intercellular adhesion
  7. Proteolysis
  8. Inflammatory responses
  9. Cell division
  10. Autophagy.
  11. cell motility
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3
Q

What makes up the cytoskeleton?

A
  1. Microtubules
  2. Intermediate filaments
  3. Microfilaments - actin
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4
Q

What are microtubules?

A
  1. Made of tubulin
  2. 25nm diameter
  3. Important in moving things around cells.
  4. Can be disrupted by Shigella, salmonella, and campylobacter
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5
Q

What are intermediate filaments?

A
  1. Made of cytokeratin and vimentin
  2. 10 nm diameter
  3. Less bacteria interact with these but we don’t really know why
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6
Q

What are microfilaments?

A
  1. Made of actin
  2. 7nm diameter
  3. Can be modified by lots of bacteria.
  4. Salmonella, E coli, shigella, listeria, yersinia and clostridium.
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7
Q

What are the 2 main methods of bacterial entry into cells?

A
  1. Trigger method eg salmonella
  2. Zipper method eg listeria
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8
Q

What is the common thing between the trigger and zipper method of entry?

A
  1. They involve rearrangements of the actin cytoskeleton.
  2. This is controlled by Rho GTPases and inositol phosphate metabolism.
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9
Q

What is the trigger method of bacterial entry?

A
  1. Bacteria use a type 3 secretion system to transfer proteins into the host cell.
  2. These proteins trigger cellular responses that manipulate actin in the cell.
  3. This causes large membrane ruffles that then take up the bacteria.
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10
Q

What is the zipper method of bacterial entry?

A
  1. Adhesion molecule and host receptor interactions trigger proteins in the host cell to change.
  2. This alters the cytoskeleton to change and take up the bacteria.
  3. InL A interacts with E-cadherin.
  4. InL B interacts with the Met receptor which recruits adaptor proteins to interact with actin and phosphatidylinositol .
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11
Q

How does salmonella enter host cells?

A
  1. Salmonella is a good regulator of the cytoskeleton.
  2. It changes the cell by manipulating actin.
  3. Formation of membrane ruffles happens really quickly. About 20-40 secs
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12
Q

What is the main regulator of the actin cytoskeleton?

A

Rho GTPases

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13
Q

What are the 3 main Rho GTPases?

A
  1. Rho
  2. Rac
  3. Cdc42
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14
Q

What does constitutive expression of the 3 Rho GTPases cause?

A

Rho - stress fibres
Rac - Lamellopodia
Cdc42 - Filopodia

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15
Q

What family does Rho GTPases belong to?

A

The Ras superfamily

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16
Q

How are Rho GTPases regulated?

A
  1. They are active when bound to GTP.
  2. They are inactive when bound to GDP.
  3. Guanine nucleotide exchange factors (GEFs) exchange GDP for GTP to activate Rho.
  4. GTPase-activating proteins (GAPs) hydrolyse GTP to GDP to inactivate Rho.
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17
Q

How can bacteria manipulate Rho GTPase activity?

A
  1. They can have mimics of GEFs and GAPs.
  2. They can have proteins that regulate host GEFs and GAPs
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18
Q

What bacterial proteins mimic GEFs to activate Rho GTPase activity?

A
  1. Salmonella SopE/SopE2
  2. Burkholderia pseudomallei BopE.
  3. Enteropathogenic E coli Map
  4. Shigella IpgB1/IpgB2
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19
Q

What bacterial proteins mimic GAPs to deactivate Rho GTPase activity?

A
  1. Salmonella SptP
  2. Yersinia YopE
  3. Pseudomonas Exo T and Exo S.
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20
Q

Why are bacterial GAP mimics important?

A
  1. They are important so the bacteria doesn’t overstimulate the host cell
  2. This promotes survival
21
Q

How does salmonella manipulate Rho GTPases and actin for infection?

A
  1. Salmonella is reliant on actin rearrangement for infection.
  2. SopE and SopE2 are GEFs that activate Rac1 and Cdc42.
  3. This induces lamellipodia and filopodia.
  4. It also secrets SptP to switch off the Rho GTPases.
22
Q

What is a secondary function of salmonella’s SopE2?

A
  1. It can make host cells less susceptible to further invasion.
  2. It helps salmonella create its own niche and keep other bacteria out.
23
Q

What other ways can bacterial regulate Rho GTPases?

A
  1. Mostly through post translational modifications.
  2. ADP-ribosylation, glucosylation, deamination and proteolysis.
  3. These can switch on or off Rho GTPases.
24
Q

What are some examples of other regulators of Rho GTPases?

A
  1. ADP-ribosylation by clostridium, bacillus and S. aureus.
  2. Glucosylation by C. diff toxins A and B.
  3. Deamination/ transglutamination by E coli and bordetella.
  4. Proteolysis by Yersinia.
25
Q

What are some bacterial factors that modulate actin independently of Rho GTPases?

A
  1. ADP-ribosylation by salmonella SpvB and Aeromonas hydrophilia VgrG1.
  2. Cross-linking and stabilisation by salmonella SipA/C, shigella IpaC and vibrio cholerae VgrG1.
    3 E coli SPATE toxins cleave fodrin to modulate actin.
26
Q

What is the mechanism of actin polymerisation used to form membrane ruffles?

A
  1. Rho GTPases or PIP2 activate WASP proteins.
  2. WASP proteins tightly control actin polymerisation and are auto-inhibited until released by Rho GTPases.
  3. WASP recruits Arp2/3
  4. Arp2/3 controls the polymerisation and branching of actin.
27
Q

How can actin polymerisation be activated through tyrosine kinase signalling?

A
  1. Phosphorylated tyrosine recruits Nck via SH2 domains.
  2. Nck recruits WASP.
  3. WASP recruits Arp2/3
  4. This alters actin.
  5. This recruitment is important for bacteria that make actin tails for movement.
28
Q

What are the different mimics bacteria can used to recruit Arp2/3 and make actin tails?

A
  1. Listeria’s ActA mimics WASP directly to recruit Arp2/3.
  2. Rickettsia’s TickA is also a WAPS mimic.
  3. Shigella has an adaptor protein that recruits host cell WASP to recruit Arp2/3.
  4. Vaccina virus has a protein that can be tyrosine phosphorylated to recruit Nck. This recruits WASP and then Arp2/3.
  5. The end result of all these is the same.
29
Q

How does enteropathogenic E.coli recruit Arp2/3 to make actin pedestals?

A
  1. It has a type 3 secretion system that transfers Tir to the host cell membrane.
  2. E coli has a surface protein called intimin that binds to Tir on the host cell membrane.
  3. This is critical for pedestal formation.
  4. The intimin/Tir interaction mimics that tyrosine phosphorylation point in the process to recruit Nck, WASP and Arp2/3.
30
Q

What happens to intracellular bacteria once they enter the host cell?

A
  1. Some escape the endosome.
  2. Some prevent endosome fusion with the lysosome.
  3. Some survive in the phagolysosome.
31
Q

How can bacteria prevent endosomal maturation in a cell?

A
  1. Bacteria can alter the early endosome to prevent late endosome development
  2. Bacteria can alter the late endosome to prevent lysosome development.
  3. Both of these are mostly done by preventing fusion with lytic compartments.
32
Q

How does salmonella prevent endosomal maturation?

A
  1. Once salmonella is in the cell it turns on another Type 3 secretion system to maintain its replicative niche.
  2. Salmonella ends up near the Golgi after being driven along microtubules.
  3. Along the way the endolytic compartment interacts with the early endosome but it doesn’t fully interact with the late endosome.
  4. It means it avoids further maturation into a lysosome.
33
Q

How are intracellular compartments defined?

A

by the phosphatidylinositol lipids that are in its membrane.

34
Q

How can bacteria modify the compartments they are in?

A

By changing the Phosphatidylinositol lipids in its membrane.

35
Q

What can the number of phosphate groups in the inositol ring determine?

A
  1. What the compartment can interact with.
  2. What can bind the compartment.
  3. The proteins in their membrane.
36
Q

What phosphatidylinositol lipids define the plasma membrane?

A
  1. Pi45P2
  2. Pi345P3
  3. Pi4P
37
Q

What phosphatidylinositol lipids define the early endosome membrane?

38
Q

What phosphatidylinositol lipids define the late endosome membrane?

39
Q

What is an important stage in the maturation of the endosome to the late endosome?

A

The switch from Pi3P to Pi35P2

40
Q

Why do salmonella and shigella cleave PI(4,5)P2?

A
  1. SigD and IpgD are inositol phosphatases that cleave PI(4,5)P2.
  2. This cleavage is important in the formation of the initial vacuole that takes up salmonella and shigella.
  3. If this doesn’t happen the vacuoles get covered in actin and the bacteria cannot traffic properly in the cell.
41
Q

How does salmonella interact with the phosphatidylinositol lipids in the endosome?

A
  1. When salmonella invades cells, they get loads of Pi3P in the early endosome.
  2. Salmonella actively maintains Pi3P on the salmonella endosome to prevent maturation to a late endosome.
42
Q

What organisms can interact with the phosphatidylinositol lipid pathways?

A
  1. TB
  2. Salmonella
  3. Shigella
  4. Vaccina virus
43
Q

What is membrane trafficking?

A
  1. A complex process.
  2. Involves endocytosis, exocytosis and vesicle trafficking.
  3. Phosphatidylinositol lipids drive trafficking and maturation
  4. Rab and Arf are GTPases important in vesicle fusion.
  5. SNAP and SNARE proteins are also important.
44
Q

What bacterial proteins can regulate Arf GTPases to manipulate membrane trafficking during infection?

A
  1. Normally GEFs and GAPs.
  2. Legionella pneumophilia RalF
  3. Rickettsia RalF
  4. Shigella Flexneri IpgD
45
Q

What bacterial proteins can regulate Rab GTPases to manipulate membrane trafficking during infection?

A
  1. Legionella pheumophilia SidM, LepB and SidD
  2. Pseudomonas aeruginosa ExoS.
  3. Salmonella GtgE.
46
Q

What bacteria can end up in an ER-like compartment?

A
  1. Legionella
  2. Brucella
47
Q

How does legionella end up in an ER-like compartment?

A
  1. Legionella has a type 4 secretion system that transfers over 100 different effector proteins to the host.
  2. Assumed that all these have regulatory functions in the host cell.
  3. These have a subtle effect on efficiency on infection.
  4. It blocks the development into a late endosome.
  5. It recruits ER proteins to look like an additional ER compartment.
48
Q

How does Brucella end up in an ER-like compartment?

A
  1. It has a type 4 secretion system that modulates the phagosome.
  2. It alters intracellular trafficking in the infected cell.
  3. It blocks late endosome development and recruits ER proteins to look like the ER.

Frontiers in infectious diseases (16 decks)

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