Fig. 1

ACS and ACL are essential to produce acetyl-CoA in the cytosol and nucleus. a Schematic representation of the metabolic pathways in T. gondii for acetyl-CoA production and transport into the cellular compartments where it is required: the apicoplast, mitochondrion, cytosol, nucleus and the endoplasmic reticulum (ER). Metabolic pathways are highlighted in blue and enzymes in red, and metabolites are depicted in black. BCKDH, branched-chain α-keto acid dehydrogenase-complex; PDC, pyruvate dehydrogenase complex; FA, fatty acid; FASII, type II FA synthase, ACL, ATP citrate lyase; ACS, acetyl-CoA synthetase; AT1, acetyl-CoA transporter; ER, endoplasmic reticulum; TCA, tricarboxylic acid. b Table highlighting the essentiality [10, 11] of acetyl-CoA-generating enzymes in T. gondii (Tgo) and Plasmodium berghei (Pbe) and their conservation across different apicomplexans. c Immuno-blot of total protein lysates from iΔACS (left panel) and ΔACL/iΔACS parasites (right panel) for which Shield-1 (Shld-1) was removed at several time points prior to egress to test protein regulation. Western blots were probed using α-myc antibody to detect the myc-tag of DD-ACS, and α-profilin (PRF) was used as a loading control. d Plaque assays were performed by inoculating human foreskin fibroblast (HFF) monolayers with either iΔACS, or ΔACL/iΔACS parasite strains and left to grow in the presence (+) or absence (−) of Shld-1 over a period of 7 days. Plaques were revealed by crystal violet staining of infected HFF monolayers