Gliding motility: An efficient mechanism for cell penetration

  title={Gliding motility: An efficient mechanism for cell penetration},
  author={L. David Sibley and Sebastian H{\aa}kansson and Vern B. Carruthers},
  journal={Current Biology},

Figures from this paper

Bacterial motility: Secretory secrets of gliding bacteria

Role of Toxoplasma gondii Myosin A in Powering Parasite Gliding and Host Cell Invasion

A genetic screen to generate a tetracycline-inducible transactivator system in T. gondii caused severe impairment in host cell invasion and parasite spreading in cultured cells, and unambiguously established the pathogenic function of this motor in an animal model.

Proteases as potential targets for blocking Toxoplasma gondii invasion and replication

This chapter reviews the recent developments in the characterization of T. gondii proteases and protein substrates and discusses potential opportunities for impairing invasion and replication by specifically blocking proteolytic processing events.

Cytoskeleton of Apicomplexan Parasites

The unusual properties of actin and myosin in the Apicomplexa, the highly stereotyped microtubule populations in apicOMplexans, and a network of recently discovered novel intermediate filament-like elements in these parasites are discussed.



Cell motility of sporozoan protozoa.

Host cell invasion by Apicomplexa: an expression of the parasite's contractile system?

It is suggested that the parasite enters the parasitophorous vacuole by ‘capping’ the host/parasite junction down its body, so locomoting into the host cell, and the specificity of membrane receptors would enable the one membrane-associated contractile system to be responsible for locomotion, antibody capping and host cell invasion.

TRAP Is Necessary for Gliding Motility and Infectivity of Plasmodium Sporozoites

Participation of myosin in gliding motility and host cell invasion by Toxoplasma gondii

Results indicate that myosin probably participate(s) in powering gliding motility, a process that is essential for cell invasion by T. gondii.

Sequential protein secretion from three distinct organelles of Toxoplasma gondii accompanies invasion of human fibroblasts.

Compared the kinetics of secretion from these different compartments during host cell invasion using immunofluorescence, immunoelectron microscopy, and quantitative immunoassays, it is suggested that their release is governed by separate signals and that their contents mediate distinct phases of intracellular parasitism.

Malaria sporozoites leave behind trails of circumsporozoite protein during gliding motility.

The fact that the CS protein is an exoantigen continuously released as trails by motile sporozoites, together with the previous finding that anti-CS protein antibodies inhibit sporozoite motility, strongly suggests that theCS protein plays a role in gliding motility.

The role of the cytoskeleton in the motility of coccidian sporozoites.

This proposed model for motility of coccidia sporozoites is consistent with all current observations on cell invasion by the sporozoa and therefore suggests that locomotion is an integral component of host cell invasion in this group of parasites.

Actin-Based Cell Motility and Cell Locomotion

Actin in the parasite Toxoplasma gondii is encoded by a single copy gene, ACT1 and exists primarily in a globular form.

The ACT1 gene is characterized and the conventional isoform of actin that it encodes within T. gondii tachyzoites is localized, indicating that actin exists primarily in a globular form in T. Gondii.