Table 1

GeneFunctionOrganism (Gene ID)Experimental dataRef.

BER Genes

Uracyl-DNA glycosylase
(UNG)
Excision of uracil in DNAT. cruzi (Tc00.1047053511277.330)(i) In vitro activity (enhanced by AP endonuclease)[16, 17]
(ii) Heterologous complementation of E. coli

AP endonuclease1Cleavage of the phosphodiester bond at the 5 side of AP siteT. cruzi (Tc00.1047053507083.30)(i) Heterologous complementation of E. coli [18]
L. major (LmjF16.0680)(i) Heterologous complementation of E. coli [1820]
(ii) Increment of H 2 O 2 and methotrexate resistance

POL 𝛽 Polymerization of DNA
Strand displacement (long-patch)
Cleavage of the 5 - dRP
T. cruzi (Tc00.1047053503955.20)(i) In vitro activity
(ii) Kinetoplast localization
[21]
T. brucei (Tb927.5.2780)[22]

PARPBinding to ssDNA
Stimulation of DNA synthesis and strand displacement
T. cruzi (Tc00.1047053509721.60)(i) In vitro activity (enhanced by SSB)[23]

NER Genes

TFIIH-TFB1Component of TFIIHT. brucei (Tb11.01.1200)(i) Essential for initiating synthesis of spliced leader RNA
TFIIH-TFB2T. brucei (Tb927.10.5210)
TFIIH-TFB4T. brucei (Tb11.01.7730)[24]
TFIIH-TFB5T. brucei (Tb10.61.2600)

TFIIH-XPBComponent of TFIIH (helicase)T. brucei (Tb11.01.7950Tb927.3.5100)(i) Interaction with TSP1 and TSP2
TFIIH-XPDT. brucei (Tb927.8.5980)(i) Nuclear localization
TFIIH-TSP1Trypanosomatid-specific component of TFIIHT. brucei (Tb927.1.1080)(i) Essential for initiating synthesis of spliced leader RNA[24]
TFIIH-TSP2T. brucei (Tb11.01.5700)(i) Nuclear localization
(ii) Essential for initiating synthesis of spliced leader RNA

XAB 2 May function as a scaffold for protein complex formationT. cruzi (Tc00.1047053509767.40)(i) Putative
T. brucei (Tb927.5.1340)(i) Putative
L. major (LmjF23.1550)(i) Putative

MMR Genes

MSH2 Repair of single base-base and IDL mismatches
Heterodimers with MSH3 or MSH6
T. cruzi (Tc00.1047053507711.320)(i) Three isoforms with different efficiencies[25, 26]
(ii) Involvement in oxidative stress response (independently from MLH1)
T. brucei (Tb927.10.11020)(i) Involvement in oxidative stress response (independently from MLH1)[2628]
(ii) Microsatellite instability and MNNG tolerance in MSH2/MLH1 double mutants
(iii) Regulatory role in HR

MLH1Heterodimers with MutL homologs
Matchmaker for coordinating eventes from mismatch binding to DNA synthesis
(i) Microsatellite instability and MNNG tolerance in MSH2/MLH1 double mutants
(ii) Regulatory role in HR
T. brucei (Tb927.8.6840)[27, 28]

NHEJ Genes

Ku70DSB recognitionT. brucei (Tb927.3.5030)(i) Telomere maintenance[29, 30]
DSB bridging nucleolytic processing of the ends
Ku80Telomere maintenanceT. brucei (Tb927.6.1760)

HR Genes

Mre11DSB end resectionT. brucei (Tb927.2.4390)(i) Mre11 mutations cause impairment of HR and increased DNA damage sensitivity[31, 32]
Nuclease activities
Rad51Recombinases(i) Gene expression induced by DNA damaging agents
(ii) Involved in DSBs and oxidative lesions repair
T. cruzi (Tc00.1047053503801.30)[33]
T. brucei (Tb11.01.0360)(i) Null mutants led to impairments in VSG switch and DNA transformation, besides a higher sensitivity to genotoxic agents[34]
L. major (LmjF28.0550)(i) Gene expression induced by DNA-damaging agents[35]

Dmc1RecombinasesT. brucei (Tb09.211.1210)(i) DMC1 mutation does not affect HR or VSG switching[36]

BRCA2ssDNA binding
Recombination mediator
T. brucei (Tb927.1.640)(i) Expansion in the number of BRC repeats
(ii) BRCA2 mutants display antigenic variation impairment and genome instability
[37]

Rad51-3 ssDNA binding
Recombination mediator activity
T. brucei (Tb11.02.0150)(i) Rad51-3 mutations resulted in reduced levels of VSG switching, altered RAD51 localization following DNA damage and DNA damage sensitized parasites[38]
Rad51-5T. brucei (Tzb10.389.1770)(i) Rad51-5 mutations caused altered RAD51 localization following DNA damage and DNA damage sensitized parasites[38]

TLS Genes

Pol 𝜂 Error-free bypass of cis-syn cyclobutane pyrimidine dimers (CPDs)T. cruzi (Tc00.1047053511911.120)(i) Heterologous complementation of S. cerevisae
(ii) In vitro bypass of 8-oxoG
(iii) Overexpression increases H 2 O 2 resistance
[39]

Pol 𝜅 Bypass of N2-adducted dG lesions
Extension of mismatched primer termini
T. cruzi (Tc00.1047053503755.30)(i) Mitochondrial localization
(ii) In vitro bypass of8-oxoG
(iii) DNA synthesis within recombination intermediates
(iv) Overexpression increases zeocin, gamma radiation, and H 2 O 2 resistance
[40]