Surface attachment, promoted by the actomyosin system of Toxoplasma gondii is important for efficient gliding motility and invasion View Full Text


Ontology type: schema:ScholarlyArticle      Open Access: True


Article Info

DATE

2017-01-18

AUTHORS

Jamie A. Whitelaw, Fernanda Latorre-Barragan, Simon Gras, Gurman S. Pall, Jacqueline M. Leung, Aoife Heaslip, Saskia Egarter, Nicole Andenmatten, Shane R. Nelson, David M. Warshaw, Gary E. Ward, Markus Meissner

ABSTRACT

BackgroundApicomplexan parasites employ a unique form of movement, termed gliding motility, in order to invade the host cell. This movement depends on the parasite’s actomyosin system, which is thought to generate the force during gliding. However, recent evidence questions the exact molecular role of this system, since mutants for core components of the gliding machinery, such as parasite actin or subunits of the MyoA-motor complex (the glideosome), remain motile and invasive, albeit at significantly reduced efficiencies. While compensatory mechanisms and unusual polymerisation kinetics of parasite actin have been evoked to explain these findings, the actomyosin system could also play a role distinct from force production during parasite movement.ResultsIn this study, we compared the phenotypes of different mutants for core components of the actomyosin system in Toxoplasma gondii to decipher their exact role during gliding motility and invasion. We found that, while some phenotypes (apicoplast segregation, host cell egress, dense granule motility) appeared early after induction of the act1 knockout and went to completion, a small percentage of the parasites remained capable of motility and invasion well past the point at which actin levels were undetectable. Those act1 conditional knockout (cKO) and mlc1 cKO that continue to move in 3D do so at speeds similar to wildtype parasites. However, these mutants are virtually unable to attach to a collagen-coated substrate under flow conditions, indicating an important role for the actomyosin system of T. gondii in the formation of attachment sites.ConclusionWe demonstrate that parasite actin is essential during the lytic cycle and cannot be compensated by other molecules. Our data suggest a conventional polymerisation mechanism in vivo that depends on a critical concentration of G-actin. Importantly, we demonstrate that the actomyosin system of the parasite functions in attachment to the surface substrate, and not necessarily as force generator. More... »

PAGES

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Identifiers

URI

http://scigraph.springernature.com/pub.10.1186/s12915-016-0343-5

DOI

http://dx.doi.org/10.1186/s12915-016-0343-5

DIMENSIONS

https://app.dimensions.ai/details/publication/pub.1024313095

PUBMED

https://www.ncbi.nlm.nih.gov/pubmed/28100223


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32 schema:description BackgroundApicomplexan parasites employ a unique form of movement, termed gliding motility, in order to invade the host cell. This movement depends on the parasite’s actomyosin system, which is thought to generate the force during gliding. However, recent evidence questions the exact molecular role of this system, since mutants for core components of the gliding machinery, such as parasite actin or subunits of the MyoA-motor complex (the glideosome), remain motile and invasive, albeit at significantly reduced efficiencies. While compensatory mechanisms and unusual polymerisation kinetics of parasite actin have been evoked to explain these findings, the actomyosin system could also play a role distinct from force production during parasite movement.ResultsIn this study, we compared the phenotypes of different mutants for core components of the actomyosin system in Toxoplasma gondii to decipher their exact role during gliding motility and invasion. We found that, while some phenotypes (apicoplast segregation, host cell egress, dense granule motility) appeared early after induction of the act1 knockout and went to completion, a small percentage of the parasites remained capable of motility and invasion well past the point at which actin levels were undetectable. Those act1 conditional knockout (cKO) and mlc1 cKO that continue to move in 3D do so at speeds similar to wildtype parasites. However, these mutants are virtually unable to attach to a collagen-coated substrate under flow conditions, indicating an important role for the actomyosin system of T. gondii in the formation of attachment sites.ConclusionWe demonstrate that parasite actin is essential during the lytic cycle and cannot be compensated by other molecules. Our data suggest a conventional polymerisation mechanism in vivo that depends on a critical concentration of G-actin. Importantly, we demonstrate that the actomyosin system of the parasite functions in attachment to the surface substrate, and not necessarily as force generator.
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39 G-actin
40 Recent evidence
41 ResultsIn
42 T. gondii
43 Toxoplasma gondii
44 actin
45 actin levels
46 actomyosin system
47 attachment
48 attachment sites
49 cells
50 collagen-coated substrates
51 compensatory mechanisms
52 completion
53 complexes
54 components
55 concentration
56 conditional knockout
57 conditions
58 core component
59 critical concentration
60 cycle
61 data
62 different mutants
63 efficiency
64 evidence
65 exact molecular role
66 exact role
67 findings
68 flow conditions
69 force
70 force generator
71 force production
72 form
73 formation
74 function
75 generator
76 gliding
77 gliding motility
78 gondii
79 host cells
80 important role
81 induction
82 invasion
83 kinetics
84 knockout
85 levels
86 lytic cycle
87 machinery
88 mechanism
89 molecular role
90 molecules
91 motility
92 movement
93 mutants
94 order
95 parasite actin
96 parasite actomyosin system
97 parasite functions
98 parasite movement
99 parasites
100 percentage
101 phenotype
102 point
103 polymerisation kinetics
104 polymerisation mechanism
105 production
106 role
107 sites
108 small percentage
109 speed
110 study
111 substrate
112 subunits
113 surface attachment
114 surface substrate
115 system
116 unique form
117 vivo
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