Mutant/mutation
The mutant expresses a GFP-tagged version of MyoA

Protein (function)
Myosin A is the founding member of unconventional class XIV myosins. These myosins are remarkably small, essentially composed of the actin-interacting ATPase domain, followed by a very short tail domain. Class XIV myosins are exclusively found in the Alveolata branch of eukaryotic organisms, including the Apicomplexa. Plasmodium Myosin A is considered vital for merozoite invasion of erythrocytes. Myosin A is a component of the glideosome of apicomplexan parasites, which is an actin- and myosin-based machine located at the pellicle, between the plasma membrane (PM) and inner membrane complex (IMC), that powers parasite motility, migration, and host cell invasion and egress. It is composed of myosin A, its light chain MLC1, and two gliding-associated proteins, GAP50 and GAP45

Myosin A (MyoA) is a Class XIV myosin implicated in gliding motility and host cell and tissue invasion by malaria parasites. MyoA is part of a membrane-associated protein complex called the glideosome, which is essential for parasite motility and includes the MyoA light chain MTIP, and several glideosome-associated proteins (GAPs).  We examined MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and insect hosts. In extracellular ookinetes, sporozoites and merozoites, MyoA was located at the parasite periphery. In the sexual stages, zygote formation and initial ookinete differentiation precede MyoA synthesis and deposition, which occurred only in the developing protuberance. In developing intracellular asexual blood stages, MyoA was synthesized in mature schizonts and was located at the periphery of segmenting merozoites, where it remained throughout maturation, merozoite egress and host cell invasion.

Phenotype
From the Abstract: 'We examined MyoA expression throughout the Plasmodium berghei life cycle in both mammalian and insect hosts. In extracellular ookinetes, sporozoites and merozoites, MyoA was located at the parasite periphery. In the sexual stages, zygote formation and initial ookinete differentiation precede MyoA synthesis and deposition, which occurred only in the developing protuberance. In developing intracellular asexual blood stages, MyoA was synthesized in mature schizonts and was located at the periphery of segmenting merozoites, where it remained throughout maturation, merozoite egress and host cell invasion.'

Using live parasite microscopy, the protein was detected uniformly at the periphery of segmenting schizonts and extracellular merozoites in asexual blood stages and at a similar location in extracellular ookinetes and salivary gland sporozoites, consistent with location at the IMC.

MyoA-GFP was not visible in either activated or non-activated gametocytes and barely detectable in the zygote and stage I and II ookinetes. Following the establishment of morphological polarity at about 10 hours after fertilization (Stage III) the protein was detectable in the growing protuberance rather than the spherical body in the intermediate retort forms, so-called because of their shape (stages III–V). This location was retained in later stages, with the MyoA-GFP associated with the parasite periphery in fully formed motile ookinetes. There was a concentration of fluorescence detected at the apical tip of the mature ookinete.

In sporozoites there was also a clear perinuclear localization.
In early cytomere stages of liver-stage schizonts the fluorescence signal appeared to be cytosolic, rather than membrane associated. In late cytomere stages, 55 h after invasion by sporozoites, a clear peripheral location associated with the hepatic merozoites was observed.

Additional information
Tagging MyoA with GFP resulted in no detectable phenotype: there was no effect on the rate of asexual parasite growth, on male gametogenesis (the number of exflagellation centres), the number of oocysts per mosquito gut or the efficiency of infection via sporozoite inoculation (as judged by the number of days following infected mosquito bite that parasites were observed by microscopy in blood smears).

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