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Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1
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SYSNO ASEP 0498799 Druh ASEP J - Článek v odborném periodiku Zařazení RIV J - Článek v odborném periodiku Poddruh J Článek ve WOS Název Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1 Tvůrce(i) Procházková, Michaela (BC-A) RID
Panicucci, Brian (BC-A)
Zíková, Alena (BC-A) RID, ORCIDCelkový počet autorů 3 Číslo článku 5135 Zdroj.dok. Scientific Reports. - : Nature Publishing Group - ISSN 2045-2322
Roč. 8, MAR 23 (2018)Poč.str. 15 s. Forma vydání Online - E Jazyk dok. eng - angličtina Země vyd. GB - Velká Británie Klíč. slova PEPTIDYL-TRANSFER-RNA ; RIBOSOMAL-PROTEIN S12 ; HUMAN ATP SYNTHASE ; LEISHMANIA-TARENTOLAE ; KINETOPLAST DNA ; ALTERNATIVE OXIDASE ; SECONDARY STRUCTURE ; ADP/ATP CARRIER ; MAXICIRCLE DNA ; INNER MEMBRANE Vědní obor RIV EE - Mikrobiologie, virologie Obor OECD Microbiology CEP LL1205 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy EF16_019/0000759 GA MŠMT - Ministerstvo školství, mládeže a tělovýchovy Institucionální podpora BC-A - RVO:60077344 UT WOS 000428163600006 EID SCOPUS 85044397257 DOI 10.1038/s41598-018-23472-6 Anotace 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. Pracoviště Biologické centrum (od r. 2006) Kontakt Dana Hypšová, eje@eje.cz, Tel.: 387 775 214 Rok sběru 2019 Elektronická adresa https://www.nature.com/articles/s41598-018-23472-6
Počet záznamů: 1