Mutant/mutation
The mutant lacks expression of Scd and and lacks a drug-selectable marker.
To generate a Scd KO drug-selectable marker free (MF) parasite line, Scd KO schizonts of mutant RMgm-5550 were transfected with the EcoRV/NotI-digested Scd targeting cassette to remove the hdhfr/yfcu drug-selectable marker cassette.

Protein (function)
The malaria parasite can modify fatty acids, and stearoyl-CoA Δ9-desaturase (Scd) is an enzyme that catalyzes the synthesis of oleic acid by desaturation of stearic acid. Plasmodium parasites can modify de novo synthesized or scavenged fatty acids into long unsaturated fatty acids. An endoplasmic reticulum (ER)-localized stearoyl-CoA desaturase (Scd) was identified in P. falciparum that catalyzes the formation of oleic acid from stearic acid by the insertion of a cis double bond at the Δ9 position of fatty acyl-CoAs.

Phenotype
Scd KO sporozoites infect the liver but fail to establish blood-stage infections in mice.
Rare breakthrough infections in mice are only observed after infecting mice with higher sporozoite doses.
See mutant RMgm-5550 for a more detailed analysis of the phenotype of mutant parasites lacking expression of SCD1.

Additional information
To overcome the rare breakthrough infection in mice inoculated with higher doses of Scd ko (RMgm-5550) or Scot1 KO (RMgm-5587) sporozoites, a mutant with dual gene deletion (Scd/Scot1 KO; RMgm-5629) was generated.
First the Scd KO marker free (MF) parasite line (RMgm-5628) was generated by transfecting Scd KO schizonts of mutant RMgm-5550 with the EcoRV/NotI-digested Scd targeting cassette to remove the hdhfr/yfcu drug-selectable marker cassette. Next, the Scd KO (MF) schizonts were transfected with a Scot1 gene-deletion construct (see mutant RMgm-5587).

Other mutants