Myosin A expressions in sporogonic stages of Plasmodium.

Invasive stages of apicomplexan parasites are polarised cells with a highly conserved sub-cellular organisation and exhibit a unique form of locomotion termed gliding motility. Gliding motility is a substrate-dependent form of forward movement without obvious cell deformation, involving surface and cytoskeletal molecules. Current models propose that whilst cell surface molecules (thrombospondin-related adhesive protein [TRAP]-like molecules) adhere to the substratum, the parasite’s actin–myosin motor generates the force that propels the cell forward, leaving a trail of membranous material behind. There is accumulating evidence that not only cell locomotion but also host cell invasion is accomplished by gliding motility. The model proposed by Russell, that host cell invasion by apicomplexan parasites is an active process driven by the parasite’s rather than the host cell’s actin cytoskeleton, was substantially supported by re-ports on inhibition of Toxoplasma cell invasion by cytochalasin, which depolymerises and caps actin. We have cloned part of a P. berghei myosin gene (Pbmyo-A) using a polymerase chain reaction (PCR)-based approach. Amino acid (aa) sequences of TgM-A, TgM-B, TgM-C and of Pfmyo-1 were aligned, and degenerate primers were designed from highly conserved regions. The aa sequence (735 aa) deduced from the partial P. berghei gene sequence confirmed that the molecule belongs to the new class XIV of unconventional myosins described in T. gondii and P. falciparum. The P. falciparum myo-A gene was obtained from cDNA of asexual stages whereas the major part of the P. berghei gene was cloned from mRNA purified from ookinetes suggesting that myosin-A may be expressed by different invasive stages of malaria parasites.