Theft of Host Transferrin Receptor-1 by Toxoplasma gondii is Required for Infection: MS Proteome of Purified T. gondii Tachyzoites

ABSTRACT: Host nutrient acquisition is essential for apicomplexan parasite infection, yet mechanisms underpinning this are not defined. We discovered the genome of Toxoplasma gondii lacks conserved genes for iron transport and storage and show these host cell proteins including the transferrin receptor 1, transferrin, ferritin heart/heavy and liver/light chains, and clathrin light chain are robustly taken up by tachyzoites. Acquisition of these host cell proteins was conserved across host cell species and parasite virulence type. Increased trafficking of host cell transferrin receptor 1 to endolysosomes boosted tachyzoite acquisition of host proteins and growth rate. Bradyzoites possessed little capacity to acquire host cell proteins consistent with the cyst wall representing a barrier to host cell protein cargo. The accompanying study to this dataset provides insight into essential functions associated with parasite theft of host iron acquisition and storage proteins. This dataset is proteomic analysis from purified T. gondii tachyzoites analyzed with both human and T. gondii databases to assess retention of human protein within T. gondii bodies.

INSTRUMENT(S):

ORGANISM(S): Homo Sapiens (human) Toxoplasma Gondii Toxoplasma Gondii Rh

TISSUE(S): Cell Culture, Fibroblast

SUBMITTER: Jason Gigley  

LAB HEAD: Jason P. Gigley

PROVIDER: PXD084269 | Pride | 2026-10-01

REPOSITORIES: Pride