Mutant/mutation
The mutant lacks expression of akratin and expresses GFP under control of the constitutive hsp70 promoter. The mutant does not contain a drug selectable marker (SM). The SM has been removed by negative selection
Published in bioRxiv preprint doi: https://doi.org/10.1101/2020.09.29.318857.

Protein (function)
PbANKA_1105300 was found to be conserved among Plasmodium spp. It shares 82% identity with its orthologue in P. yoelii, but only 35% and 32% with its orthologues in P. falciparum and P. vivax, respectively. In contrast to P. berghei and P. falciparum, the orthologues in P. yoelii and P. vivax are predicted to contain only two TMDs. Furthermore, the P. falciparum protein contains about 181 two times more amino acids than the P. berghei protein. No orthologue was found outside Plasmodium spp

Phenotype
Reduction in blood stage growth from around 10 as observed for wild type parasites to seven for parasites lacking akratin. A strong reduction in male exflagellation. Reduced gametocyte to ookinete conversion rates. 

Additional information
Evidence is presented that male gamete formation is blocked. Activated males replicate their DNA and flagellar axonemes are formed, albeit non-motile that appered to be trapped within the red blood cells.

Mutation of a C-terminal motif of akratin uncoupled akratin function in gametocytes and ookinetes (see mutant RMgm-4886). In the mutant expressing mutated akratin, ookinetes were formed but no oocysts. Evidence is presented that the mutant ookinetes are defective in midgut-wall traversal.

Other mutants