Cultured bloodstream Trypanosoma brucei adapt to life without
mitochondrial translation release factor 1

J 2018

Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1

PROCHÁZKOVÁ, Michaela, B. PANICUCCI a A. ZIKOVA

Základní údaje

Originální název

Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1

Autoři

PROCHÁZKOVÁ, Michaela (203 Česká republika, garant, domácí), B. PANICUCCI (203 Česká republika) a A. ZIKOVA (203 Česká republika)

Vydání

Scientific reports, LONDON, NATURE PUBLISHING GROUP, 2018, 2045-2322

Další údaje

Jazyk

angličtina

Typ výsledku

Článek v odborném periodiku

Obor

10607 Virology

Stát vydavatele

Velká Británie a Severní Irsko

Utajení

není předmětem státního či obchodního tajemství

Impakt faktor

Impact factor: 4.011

Kód RIV

RIV/00216224:14740/18:00106576

Organizační jednotka

Středoevropský technologický institut

DOI

http://dx.doi.org/10.1038/s41598-018-23472-6

UT WoS

000428163600006

Klíčová slova anglicky

PEPTIDYL-TRANSFER-RNA; RIBOSOMAL-PROTEIN S12; HUMAN ATP SYNTHASE; LEISHMANIA-TARENTOLAE; KINETOPLAST DNA; ALTERNATIVE OXIDASE; SECONDARY STRUCTURE; ADP/ATP CARRIER; MAXICIRCLE DNA; INNER MEMBRANE

Štítky

rivok

Příznaky

Mezinárodní význam, Recenzováno

Změněno: 11. 3. 2019 16:03, Mgr. Pavla Foltynová, Ph.D.

Anotace

V originále

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.

Citovat

PROCHÁZKOVÁ, Michaela, B. PANICUCCI a A. ZIKOVA. Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1. Scientific reports. LONDON: NATURE PUBLISHING GROUP, 2018, roč. 8, MAR, s. 5135-5149. ISSN 2045-2322. Dostupné z: https://dx.doi.org/10.1038/s41598-018-23472-6.

@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 a A. ZIKOVA. Cultured bloodstream Trypanosoma brucei adapt to life without mitochondrial translation release factor 1. \textit{Scientific reports}. LONDON: NATURE PUBLISHING GROUP, 2018, roč.~8, MAR, s.~5135-5149. ISSN~2045-2322. Dostupné z: https://dx.doi.org/10.1038/s41598-018-23472-6.

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