Vl 7 - parasite motility Flashcards
protozoan motility I: amoeboid movement (slow) how does it work?
via lamellipodia dynamics:
1) resting state: actin under membrane
2) initial nucleation of G-actins by mDia1
3) F-actin formation
4) recruitment of WAVE and Arp2/3 complex
5) generation of branched actin network ⇒ growth of lamellapodium
What is the function of the plasmodium HSP20?
- small heat shock protein of Plasmodium
- protects F-actin
- important for adhesion and movement of sporozoites
- important during host switch
Welche Protozoen-Parasiten-Bewegungstype kennen Sie?
- Gliding motility (toxoplasm, plasmodium)
- Flagella movement (Leishmania, Plasmodium and Trypanosoma, etc.)
Ameboid movement (via lamellapodia - Ameobas, Macrophages)
In which structures can F- and G-actin be found? What can you dye them with? What is the difference between f- and G-actin?
- F- and G-actin in macropinosomes and vacuoles, adhesion plates, dot-like structures and stress fibers
- F-actin is actin in a row as a filament
- G-actin are globular single molecules of actin
- F-actin can be stained with phalloidin
- G-Aktin with Anti-Aktin-ABs
How can a flagellum be detected under an electron microscope?
Because of the 9x2 + 2 structure (with microtubulin and basal body for anchoring)
What is the muscle myosin called? And the myosin for the gliding locomotion?
Muscle myosin: Myo class II
Gliding Locomotion: Myo class XIV (only present in Apicomplexa parasites).
How does the actin-myosin-based Gliding Locomotion work?
- myosin is bound to parasite actin filaments
- also bound to TRAP-family adhesin ⇒ bind to plasma membrane and host cell receptors
- MADP + MLC interact with myosin-A
- whole structure pushed to posterior part of parasite cell ⇒ apical part of parasite cell moves forward
- Once structure reaches posterior end, the compounds are cleaved using capping enzymes
plasmodium sporozoites deposit CSP in their trail
of what do plasmodium sporozoites leave a trail?
trail of CSP ⇒ Protein secreted for gliding motility.
Which myosin class is necessary for the virulence of Apicomplexa parasites?
Myo class XIV.
How does Plasmodium invade the host cell (RBC)?
- always reorientates to apical end of merozoites independent from initial docking position
1) merozoite attachment
2) reorientation: RBC receptor + DBL/RH proteins
3) junction formation: RBC receptor + RON complex + AMA1
4) invasion: PVM formation
5) Merozoite inside cell: still interaction RBC receptor-RBC/RH, RON complex-AMA1
- remodelling of RBC via parasite proteins and organelles (PfEMP1, PSAC, KHARP, maurer’s clefts etc.)
Which cells does Toxoplasma invade?
All nuclear mammalian cells.
Name three mammalian RBC-surface proteins and their Plasmodium protein partners during merozoite invasion.
RBC receptors:
- Glycophorin A ⇒ interacts with EBA175
- Gly B ⇒ interacts with unknown protein
- Gly C ⇒ interacts with EBA140
How are new erythrocyte receptors for Plasmodium invasion identified?
Using Avexis approach to identify erythrocyte ligands for merozoite invasion.
- plate with streptavidin + bound protein (parasite)
- parasite ligands are “bait”
- host receptors (“prey”) + fluorophore or molecule that changes color upon binding/interaction added
- when host cell receptor binds to parasite protein ⇒ color change
lead to CD147 discovery
Which Plasmodium protein interacts with basigin (CD147)? What is basigine?
- Parasitic Rh5 interacts with basigin (CD147)
- essential receptor for erythrocyte invasion by Plasmodium
How many pathways to cell invasion does Plasmodium have? Which ones?
2:
- with tight juction ⇒ forms parasitophore vacuole ⇒ for efficient invasion (to stay longer in the cell).
- without tight junction ⇒ no or transient parasitophoric vacuole (to pierce cells = transmigration).
