Mutant/mutation
The mutant lacks expression of PlasMei2 and expresses the fusion gene GFP-Luciferase under control of the P. berghei eef1a promoter

Protein (function)
Regulation of mRNA translation relies on RNA binding proteins (RBPs), many of which  form complexes within the cytoplasm in entities known as processing bodies (P-bodies) or P granules. P-bodies are involved in many aspects of mRNA homeostasis including both mRNA decay and translational repression.
Mei2 was initially described in the fission yeast Schizosaccharomyces pombe, and plays a critical role in the switch from mitosis to meiosis (20). Mei2 is a member of the largest family of RBPs – those that contain a RNA recognition motif (RRM), a stretch of 70-90 amino acids that contain two consensus RNA-interacting motifs, RNP1 and RNP2. RRM-containing proteins are subdivided into ten separate families (RRM_1 thru RRM_10) based on shared amino acid identities between members of each family and Mei2 contains a C-terminal RRM_2, thought to be unique to fungi and plants.
Plasmodium contains a single Mei2-like gene (from herein referred to as PlasMei2). In the P. yoelii rodent malaria model, Plasmei2 is only expressed during liver stage development and is localized in distinct cytoplasmic structures reminiscent of P-granules
Mei2-like genes are restricted to eukaryotic genomes and fall into three broad clades, the AML and TEL groups of plants, and a fungal clade. Interestingly, PlasMei2 cannot be exclusively assigned to any one group. Yeast Mei2 contains three RRMs, two N-terminal RRM_1 domains and a C-terminal RRM_2. Only the C-terminal RRM_2 domain is present in PlasMei2.
The Plasmodium RRM_2 shows a high degree of similarity to other Mei2 RRM_2 domains, based on a comparison to representative sequences from alveolates, fungi, and plants. The RRM_2 domain shares amino acid conservation with RRMs of the Sex Lethal and HuD proteins, both of which bind single-stranded AU-rich RNA, suggesting that PlasMei2 may behave similarly.

Phenotype
Normal development/growth of asexual blood stages. Normal sporozoite production. Plasmei2‾ sporozoites failed to initiate a blood stage infection (after injection of 5x10(4) purified sporozoites). Abnormal development of liver stages. Growth arrest of late liver stages. Py plasmei2‾ liver stages increased in size in a similar manner as wildtype parasites during the course of liver stage development. IFA analysis showed no apparent aberrant phenotype of Py plasmei2‾ parasites during the first 28 hours of development. However, by 34 hours, there was evidence for abnormal development. Wildtype liver stages showed numerous nuclear centers but in the majority of Py plasmei2‾ liver stages, there was an increase in the size of a proportion of the nuclear centers, suggesting that abnormal DNA segregation was taking place. This was accompanied by an abnormal expression pattern of the endoplasmic reticulum marker, BiP, which was limited to a perinuclear localization rather than scattered expression throughout the liver stage parasite, typically observed in the wildtype liver stages at this time point. This result suggested that PlasMei2 plays an important role in liver stage endomitosis as early as 34 hours post sporozoite invasion. The phenotype was far more pronounced at the 45-hour time point, and it was clear that normal DNA segregation during endomitosis had ceased, whereas in wildtype parasites, DNA segregation, which precedes exo-erythrocytic merozoite formation, had occurred. The Py plasmei2‾ liver stage mitochondria and apicoplasts also showed signs of unusual development. In the wildtype parasite complex, branched organelle networks were present, but in the Py plasmei2‾ liver stages, the organellar network showed clear signs of abnormal development.
Maturation of liver stage parasites is characterized by cytomere formation; invaginations of the parasite plasma membrane that greatly increase membrane surface area and enable rapid formation of exo-erythrocytic merozoites by individuation throughout the exo-erythrocytic schizont Py plasmei2‾ liver stages at 43 and 48 hours of development did not show cytomere formation and did not contain mature merozoites. MSP1 expression was weak although some parasites showed strong, aggregated expression of MSP1 within the parasite.

Additional information
Evidence is presented that PlasMei2 is only expressed in liver stages. See also RMgm-1414 for a mutant expressing a cmyc-tagged version of PlasMei2. At 20 hours of liver stage development, PlasMei2  expression was not observed, However, by 32 hours of development, PlasMei2 expression was observed throughout the liver stage cytoplasm and exhibited a granular localization pattern reminiscent of P-granule localization. Localization continued to be cytoplasmic and granular as the liver stage parasite matured at both 38 and 45 hours post infection before declining to undetectable levels at 52 hours.

Other mutants
See also RMgm-1414 for a mutant expressing a cmyc-tagged version of PlasMei2.