Synthetic elevation of PI3P that induces resistance in absence of K13 mutation yields vesicle immunoproteomes enriched in signatures of proteostasis and clinical resistance. (A-B) Detection of PfEMP1 (arrow) captured by anti-ATS antibodies (but not in its absence; −1°) from PfVPS34myc and mass intensity properties of 2 replicate immunoproteomes. (C-D) Detection of PfEMP1 (arrow) captured by anti-ATS antibodies (but not in its absence; −1°) from immunoproteome from PfVPS34AAAmyc (catalytic dead enzyme in which AAA replaces the VPS34-catalytic active-site residues glutamic acid, arginine, and histidine DRH) and mass intensity properties of 2 replicate proteomes. Molecular weight standards are in kDa. (E) Comparative distribution of proteins in proteomes of VPS34myc and VPS34AAAmyc. (F) Hypergeometric analyses showing enrichment of VPS34myc immunoproteome and upregulated (but not downregulated) transcripts of the clinical artemisinin-resistant transcriptome.¹²  (G) Protein distribution analyses indicating that 95% of Pf3D7 of proteins enriched in the clinical transcriptome are present in the PfVPS34myc PfEMP1 immunoproteome. (H) Number and percentage of hits for indicated chaperone networks in the vesicle immunoproteome from PfVPSmyc reveals substantial association with reactive oxidative stress complex and T-complex chaperones also known as TCP1 ring complex of the UPR. Mu, mass units.