Fig 1.
Trypanosomatid DNA double-strand break repair and translesion synthesis machinery in the kinetoplast (left) and nucleus (right).
The kinetoplast relies on PolI-like DNA polymerases to repair double-strand breaks while the nucleus uses the full complement of homologous recombination and microhomology-mediated end-joining proteins. Oxidized bases are bypassed or repaired by different polymerases in the kinetoplast and the nucleus depending on the species of trypanosomatid.
Table 1.
Repair and translesion DNA Polymerases in Leishmania major, Trypanosoma cruzi, and Trypanosoma brucei.
Fig 2.
Double-strand break (DSB) repair pathways.
T. cruzi, T. brucei, and Leishmania spp. lack the full complement of proteins necessary to carry out NHEJ, and thus rely on HR and MMEJ for DSB repair. NHEJ, non-homologous end joining; HR, homologous recombination; MMEJ, microhomology-mediated end joining. Figure adapted from [53].
Fig 3.
Oxidative stress management in trypanosomatids and role of trypanothione.
TryS: trypanothione synthetase; TryX: tryparedoxin; rNTP: ribonucleoside triphosphate; dNTP: deoxynucleoside triphosphate; SOD: superoxide dismutase; APX: ascorbate peroxidase; RNR: ribonucleotide reductase.