Comparative Aspects of Nucleotide and Amino Acid Metabolism in Toxoplasma gondii and Other Apicomplexa

Subcellular Compartments Interplay for Carbon and Nitrogen Allocation in Chromera velia and Vitrella brassicaformis

“…2017). Of studied apicomplexans, Toxoplasma has the broadest capacity to produce amino acids de novo or secondarily from specific precursors, being auxotrophic only for Arg, His, and Trp (Chaudhary et al. 2014; Tymoshenko et al.…”

Subcellular compartments interplay for carbon and nitrogen allocation in Chromera velia and Vitrella brassicaformis

“…As yet, the primarily cytosolic localization of nitrogen metabolism in chromerids appears extraordinary among phototrophs (Allen et al 2011; Bromke 2013; de la Torre et al 2013; Dorrell et al 2017). Of studied apicomplexans, Toxoplasma has the broadest capacity to produce amino acids de novo or secondarily from specific precursors, being auxotrophic only for Arg, His and Trp (Chaudhary et al 2014; Tymoshenko et al 2015). Although the middle steps of Pro and Lys synthesis are currently unknown (Shanmugasundram et al 2013), none of these amino acid synthesis pathways appears to be placed exclusively in the apicoplast, in line with our results.…”

“…Reliance on amino acid import from the host resulted in even greater reduction of amino acid synthesis capabilities. Thus, Plasmodium synthesizes six amino acids (Gly, Glu, Gln, Pro, Asp, Asn), while Cryptosporidium , which entirely lacks an apicoplast (Keithly et al 2000; Chaudhary et al 2014), synthesizes only Gly, Glu and Pro. It is tempting to speculate that the major role of the cytosol in amino acid synthesis facilitated the plastid loss in a distantly related non-photosynthetic dinoflagellate, Hematodinium (Gornik et al 2015).…”

Polimorfismos en los genes dihidrofolatorreductasa (dhfr) y dihidropteroatosintetasa (dhps) y modelamiento estructural del gen dhps en aislamientos colombianos de Toxoplasma gondii

“…De acuerdo con la predicción obtenida mediante el modelado estructural, este polimorfismo llevaría a un cambio en la estructura secundaria, lo que podría afectar la afinidad de los antifolatos con esta enzima y estar relacionado con los cambios en la sensibilidad del parásito a estos medicamentos (29). Este cambio estructural en la afinidad de los medicamentos con la enzima parasitaria, puede llevar a que los pacientes infectados con parásitos que tienen tal polimorfismo presenten menos mejoría o tengan más recaídas debido a una menor eficacia del tratamiento.…”