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Verfasst von:Bogacz, Marta [VerfasserIn]   i
 Dirdjaja, Natalie [VerfasserIn]   i
 Wimmer, Benedikt [VerfasserIn]   i
 Habich, Carina [VerfasserIn]   i
 Krauth-Siegel, Renate [VerfasserIn]   i
Titel:The mitochondrial peroxiredoxin displays distinct roles in different developmental stages of African trypanosomes
Verf.angabe:Marta Bogacz, Natalie Dirdjaja, Benedikt Wimmer, Carina Habich, R. Luise Krauth-Siegel
E-Jahr:2020
Jahr:29 April 2020
Umfang:15 S.
Fussnoten:Gesehen am 23.07.2020
Titel Quelle:Enthalten in: Redox Biology
Ort Quelle:Amsterdam [u.a.] : Elsevier, 2013
Jahr Quelle:2020
Band/Heft Quelle:34(2020) Artikel-Nummer 101547, 15 Seiten
ISSN Quelle:2213-2317
Abstract:Hydroperoxide reduction in African trypanosomes relies on 2-Cys-peroxiredoxins (Prxs) and glutathione peroxidase-type enzymes (Pxs) which both obtain their reducing equivalents from the trypanothione/tryparedoxin couple and thus act as tryparedoxin peroxidases. While the cytosolic forms of the peroxidases are essential, the mitochondrial mPrx and Px III appear dispensable in bloodstream Trypanosoma brucei. This led to the suggestion that in this developmental stage which is characterized by a mitochondrion that lacks an active respiratory chain, only one of the two peroxidases might be required. Here we show that bloodstream cells in which the Px III gene is deleted and mPrx is down-regulated by RNA interference, proliferate as the parental cells indicating that both mitochondrial peroxidases are dispensable. However, when we raised the culture temperature to 39 °C, mPrx-depleted cells died indicating that under conditions mimicking a fever situation in the mammalian host, the protein becomes essential. In contrast, depletion of mPrx in insect stage procyclic T. brucei causes a proliferation defect under standard conditions at 27 °C, in the absence of any stress. In the absence of mPrx, a tryparedoxin-coupled roGFP2 biosensor expressed in the mitochondrial matrix is unable to respond to antimycin A treatment. Thus mPrx reduces mitochondrial H2O2 with the generation of trypanothione disulfide and acts as peroxidase. However, mPrx-depleted procyclic cells neither display any alteration in the cytosolic or mitochondrial trypanothione redox state nor increased sensitivity towards exogenous oxidative stressors suggesting that the peroxidase activity is not the crucial physiological function. After prolonged mPrx-depletion, the cells almost stop proliferation and display a highly elongated shape and diminished MitoTracker Red staining. In contrast to the situation in the mammalian bloodstream T. brucei and Leishmania, mPrx appears to play a constitutive role for the morphology, mitochondrial function and proliferation of the insect stage of African trypanosomes.
DOI:doi:10.1016/j.redox.2020.101547
URL:Bitte beachten Sie: Dies ist ein Bibliographieeintrag. Ein Volltextzugriff für Mitglieder der Universität besteht hier nur, falls für die entsprechende Zeitschrift/den entsprechenden Sammelband ein Abonnement besteht oder es sich um einen OpenAccess-Titel handelt.

Volltext: https://doi.org/10.1016/j.redox.2020.101547
 DOI: https://doi.org/10.1016/j.redox.2020.101547
Datenträger:Online-Ressource
Sprache:eng
Sach-SW:Mitochondrion
 Peroxiredoxin
 roGFP2
 Trypanosoma brucei
 Trypanothione
 Tryparedoxin
K10plus-PPN:1725374897
Verknüpfungen:→ Zeitschrift

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