Mutant/mutation
The mutant lacks expression of both Scd and Scot1.
The Scd and Scot1 double-KO (Scd/Scot1 KO) parasites were generated via double crossover homologous recombination. 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, resulting in mutant RMgm-5628. Next, the Scd KO (MF) schizonts of mutant RMgm-5628 were transfected with a Scot1 gene-deletion construct (see mutant RMgm-RMgm-5587).

Protein (function)
SCD:
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. See mutant RMgm-5550 for a more detailed analysis of the phenotype of mutant parasites lacking expression of SCD1.
SCOT1:
The Scot1 (micronemal) protein lacks a signal sequence and transmembrane domain.
See mutant RMgm-5587 for a more detailed analysis of the phenotype of mutant parasites lacking expression of SCOT1

Phenotype
Scd/Scot1 KO sporozoites infect the liver but fail to establish blood-stage infections in mice.
Evidence is presented for the following: the Scd/Scot1 KO and WT GFP parasites were indistinguishable during blood, mosquito and early liver stage development. Scd/Scot1 KO liver-stage schizonts exhibited an abnormal apicoplast biogenesis and nuclear division phenotype, failed to form hepatic merozoites, and exhibited late liver-stage arrest.
See mutant RMgm-5550 for a more detailed analysis of the phenotype of mutant parasites lacking expression of SCD1.
See mutant RMgm-5587 for a more detailed analysis of the phenotype of mutant parasites lacking expression of SCOT1

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).

From the Abstract:
'We previously generated two late liver-stage-arresting GAPs by deleting the stearoyl-CoA desaturase (Scd) or sporozoite conserved orthologous transcript 1 (Scot1) genes in Plasmodium berghei. Immunization with Scd or Scot1 GAP conferred complete protection against a sporozoite challenge. In a safety study, we observed rare breakthrough blood-stage infections in mice inoculated with high doses of sporozoites, indicating that both GAPs were incompletely attenuated. In this study, we generated a Scd/Scot1 GAP by dual gene deletion. This resulted in complete attenuation of the parasites in the liver and did not transition to blood-stage infection despite a high-dose sporozoite challenge. The Scd/Scot1 KO and WT GFP parasites were indistinguishable during blood, mosquito and early liver stage development. Moreover, Scd/Scot1 KO liver-stage schizonts exhibited an abnormal apicoplast biogenesis and nuclear division phenotype, failed to form hepatic merozoites, and exhibited late liver-stage arrest'.

Other mutants