Table 2 Key features on Trypanosoma metacaspases

S replaces the predicted catalytic C but a C is located immediately adjacent.

Absence of peptidase activity after R/D/N/K when TbMCA4 was expressed in S. cerevisiae or in E. coli.

TbMCA4 induced mitochondrial dysfunction, clonal death and growth inhibition when expressed in S. cerevisiae.

Nuclear localisation for TbMCA4.

No processing in vivo but autoprocessing for TbMCA2 after K55 and K268 in E. coli with calcium.

Class III WW domain in N-terminus of TbMCA2/3 and in C-terminus of TbMCA5.

TbMCA2 proteolytic activity: R/K-specific, Ca²⁺ dose-dependent and processing not required.

Sensitive to leupeptin, antipain, TLCK and component with R in P1 position but insensitive to E64 inhibitor.

Expression in the BSF but not in the PCF for TbMCA2/3 and in both forms for TbMCA5.

No loss-of-function phenotype detected for the triple null mutants (Δmca2/3Δmca5).

Triple RNAi induced a rapid growth arrest and a dysregulation of cytokinesis.

Colocalisation of TbMCA2/3/5 with RAB11-positive endosome but no further data support involvement of TbMCAs in cell trafficking.

TcMCA3 gene is present in 16 copies and TcMCA5 in a single copy in the T. cruzi genome.

Q/P/Y rich region in the C-terminus of TcMCA5.

Caspase-like activity concomitant with TcMCA3 nuclar relocalisation upon (FHS)-induced cell death.

Expression of TcMCA5 in epimastigote form.

Expression of TcMCA3 in the four major stages of development.

Cytoplasmic localisation and migration into the nucleus upon FHS treatment.

Epimastogotes over-expressing TcMCA5 are more sensitive to (FHS)-induced cell death.