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Due to diverse and dynamic host environments, the obligate intracellular parasite\n                      <jats:italic toggle=\"yes\">Toxoplasma gondii<\/jats:italic>\n                      must adapt to iron-limited conditions. To investigate the adaptations critical to parasite survival under these conditions, we conducted proteomic and metabolomic profiling of\n                      <jats:italic toggle=\"yes\">Toxoplasma<\/jats:italic>\n                      cultured in iron-depleted conditions. We find that iron depletion results in remodeling of the parasite proteome and triggers swift translational repression, prior to decreases in the key translational factor ABCE1. In the context of repressed translation, we also observe a significant rewiring of energy metabolism. Iron-depleted\n                      <jats:italic toggle=\"yes\">Toxoplasma<\/jats:italic>\n                      have altered mitochondrial morphology and a profound reduction in mitochondrial respiration. Untargeted metabolomics revealed changes in central carbon metabolism, with the accumulation of intermediates of glycolysis and the tricarboxylic acid (TCA) cycle. Stable isotope labeling revealed that iron deprivation leads to a fundamental disconnect between these pathways, with reduced incorporation of glucose-derived carbon into cellular macromolecules and disruption of the TCA cycle. Instead, iron-deprived parasites continued to take up glucose and maintain glycolysis for energy generation. Limiting glucose availability, either in culture media or by genetic ablation of glucose uptake, caused a significant increase in sensitivity to iron restriction. Conversely, the limitation of mitochondrially metabolized glutamine improved parasite fitness in iron-depleted conditions. Together, our results establish iron as a key regulator of parasite translation and metabolic flexibility and demonstrate an increased reliance on glycolysis for energy generation and survival under acute iron deprivation.\n                    <\/jats:p>\n                    <jats:sec>\n                      <jats:title>IMPORTANCE<\/jats:title>\n                      <jats:p>\n                        This study determines the effects of iron deprivation on the parasite\n                        <jats:italic toggle=\"yes\">Toxoplasma gondii<\/jats:italic>\n                        . Using proteomics and metabolomics, we reveal iron as a novel regulator of both protein translation and energy metabolism in\n                        <jats:italic toggle=\"yes\">Toxoplasma,<\/jats:italic>\n                        underpinning the importance of this nutrient for essential cellular processes. We find that iron depletion introduces a metabolic bottleneck, whereby parasites become dependent on glucose as their major carbon source. By modulating the parasite\u2019s metabolism by altering carbon source availability, we identify nutrient conditions that improve parasite survival under iron restriction. These data reveal a key role for adaptive plasticity of\n                        <jats:italic toggle=\"yes\">Toxoplasma<\/jats:italic>\n                        central carbon metabolism to drive survival under iron-limited conditions. Understanding the interactions between parasite nutrient availability and metabolism allows us both to map the metabolic flexibility of these parasites and identify potential vulnerabilities.\n                      <\/jats:p>\n                    <\/jats:sec>\n                  <\/jats:sec>","DOI":"10.1128\/mbio.03788-25","type":"journal-article","created":{"date-parts":[[2026,4,2]],"date-time":"2026-04-02T13:01:01Z","timestamp":1775134861000},"update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":2,"title":["Global translational and metabolic remodeling during iron deprivation in\n                    <i>Toxoplasma gondii<\/i>"],"prefix":"10.1128","volume":"17","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-1302-8905","authenticated-orcid":false,"given":"Jack C.","family":"Hanna","sequence":"first","affiliation":[{"id":[{"id":"https:\/\/ror.org\/00vtgdb53","id-type":"ROR","asserted-by":"publisher"}],"name":"Glasgow 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