PROCHÁZKOVÁ, Michaela, B. PANICUCCI and A. ZIKOVA. Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1. Scientific reports. LONDON: NATURE PUBLISHING GROUP, 2018, vol. 8, MAR, p. 5135-5149. ISSN 2045-2322. Available from: https://dx.doi.org/10.1038/s41598-018-23472-6. |
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@article{1505094, author = {Procházková, Michaela and Panicucci, B. and Zikova, A.}, article_location = {LONDON}, article_number = {MAR}, doi = {http://dx.doi.org/10.1038/s41598-018-23472-6}, keywords = {PEPTIDYL-TRANSFER-RNA; RIBOSOMAL-PROTEIN S12; HUMAN ATP SYNTHASE; LEISHMANIA-TARENTOLAE; KINETOPLAST DNA; ALTERNATIVE OXIDASE; SECONDARY STRUCTURE; ADP/ATP CARRIER; MAXICIRCLE DNA; INNER MEMBRANE}, language = {eng}, issn = {2045-2322}, journal = {Scientific reports}, title = {Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1}, volume = {8}, year = {2018} }
TY - JOUR ID - 1505094 AU - Procházková, Michaela - Panicucci, B. - Zikova, A. PY - 2018 TI - Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1 JF - Scientific reports VL - 8 IS - MAR SP - 5135 EP - 5135 PB - NATURE PUBLISHING GROUP SN - 20452322 KW - PEPTIDYL-TRANSFER-RNA KW - RIBOSOMAL-PROTEIN S12 KW - HUMAN ATP SYNTHASE KW - LEISHMANIA-TARENTOLAE KW - KINETOPLAST DNA KW - ALTERNATIVE OXIDASE KW - SECONDARY STRUCTURE KW - ADP/ATP CARRIER KW - MAXICIRCLE DNA KW - INNER MEMBRANE N2 - Trypanosoma brucei is an extracellular parasite that alternates between an insect vector (procyclic form) and the bloodstream of a mammalian host (bloodstream form). While it was previously reported that mitochondrial release factor 1 (TbMrf1) is essential in cultured procyclic form cells, we demonstrate here that in vitro bloodstream form cells can tolerate the elimination of TbMrf1. Therefore, we explored if this discrepancy is due to the unique bioenergetics of the parasite since procyclic form cells rely on oxidative phosphorylation; whereas bloodstream form cells utilize glycolysis for ATP production and FoF1-ATPase to maintain the essential mitochondrial membrane potential. The observed disruption of intact bloodstream form FoF1-ATPases serves as a proxy to indicate that the translation of its mitochondrially encoded subunit A6 is impaired without TbMrf1. While these null mutants have a decreased mitochondrial membrane potential, they have adapted by increasing their dependence on the electrogenic contributions of the ADP/ATP carrier to maintain the mitochondrial membrane potential above the minimum threshold required for T. brucei viability in vitro. However, this inefficient compensatory mechanism results in avirulent mutants in mice. Finally, the depletion of the codon-independent release factor TbPth4 in the TbMrf1 knockouts further exacerbates the characterized mitchondrial phenotypes. ER -
PROCHÁZKOVÁ, Michaela, B. PANICUCCI and A. ZIKOVA. Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1. \textit{Scientific reports}. LONDON: NATURE PUBLISHING GROUP, 2018, vol.~8, MAR, p.~5135-5149. ISSN~2045-2322. Available from: https://dx.doi.org/10.1038/s41598-018-23472-6.
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