Abstract: The ability to invade host cells is a key to the survival and pathogenicity of Apicomplexan parasites. Toxoplasma gondii is an obligatory intracellular parasite. Its motility, invasion into, and egression from host cells are powered by a machinery called acto-myosin motor （AMM）. The AMM is composed of myosin A, a myosin light chain （MLC1）, two essential light chains （ELC）1, 2 and gliding-associated protein （GAP）. The GAP family has been discovered to include GAP45, GAP50, GAP80, GAP70 and GAP40, which are the major components of glideosome that provides power for parasite motility. The glideosome of apicomplexan parasites is an actin- and myosin-based power machine located at the pellicle between the plasma membrane （PM） and inner membrane complex（IMC）. This review outlines our current understanding of GAP function and architecture as well as the molecular basis for parasite motility. Meanwhile, the use of GAPs as the candidate toxoplasmosis vaccine is prospected.

Key words: Toxoplasma gondii, Gliding-associated protein, Gliding motility, Acto-myosin motor, Glideosome