TY - JOUR
T1 - The Trypanosoma cruzi RNA-binding protein RBP42 is expressed in the cytoplasm throughout the life cycle of the parasite
AU - Tyler Weisbarth, R.
AU - Das, Anish
AU - Castellano, Paul
AU - Fisher, Michael A.
AU - Wu, Han
AU - Bellofatto, Vivian
N1 - Publisher Copyright:
© 2018, Springer-Verlag GmbH Germany, part of Springer Nature.
PY - 2018/4/1
Y1 - 2018/4/1
N2 - Trypanosoma cruzi, the protozoan parasite that causes Chagas disease in humans, has a complex life cycle that promotes survival in disparate environments. In each environment, the parasite must fine-tune its metabolic pathways to divide and multiply. In the absence of recognizable transcriptional gene regulation, it is apparent that protein levels are determined by post-transcriptional mechanisms. Post-transcriptional gene control is influenced by RNA-binding proteins that target mRNAs in the cell’s cytoplasm. To initiate the study of post-transcriptional activities in T. cruzi, we studied this organism’s ortholog of RBP42, a trypanosomal RNA-binding protein. RBP42 was originally detected in Trypanosoma brucei and was shown to target a subset of mRNAs that encode proteins governing central carbon metabolism. T. cruzi RBP42 structurally resembles T. brucei RBP42, sharing an NTF2 domain at its amino terminus and a single RNA-binding domain (specifically, the RNA recognition motif, or RRM), at its carboxy terminus. A phylogenetic analysis reveals that an NTF2 and a single RRM are distinguishing features of all RBP42 orthologs within the broad kinetoplastid grouping. T. cruzi RBP42 is expressed in all life cycle stages of the parasite as determined by immunoblot and immunofluorescence microscopy. In each case, the protein is localized to the cytoplasm, indicating a role for T. cruzi RBP42 in post-transcriptional activities in all stages of the parasite life cycle. We speculate that RBP42 influences the dynamic metabolic pathways responsible for parasite infection and transmission.
AB - Trypanosoma cruzi, the protozoan parasite that causes Chagas disease in humans, has a complex life cycle that promotes survival in disparate environments. In each environment, the parasite must fine-tune its metabolic pathways to divide and multiply. In the absence of recognizable transcriptional gene regulation, it is apparent that protein levels are determined by post-transcriptional mechanisms. Post-transcriptional gene control is influenced by RNA-binding proteins that target mRNAs in the cell’s cytoplasm. To initiate the study of post-transcriptional activities in T. cruzi, we studied this organism’s ortholog of RBP42, a trypanosomal RNA-binding protein. RBP42 was originally detected in Trypanosoma brucei and was shown to target a subset of mRNAs that encode proteins governing central carbon metabolism. T. cruzi RBP42 structurally resembles T. brucei RBP42, sharing an NTF2 domain at its amino terminus and a single RNA-binding domain (specifically, the RNA recognition motif, or RRM), at its carboxy terminus. A phylogenetic analysis reveals that an NTF2 and a single RRM are distinguishing features of all RBP42 orthologs within the broad kinetoplastid grouping. T. cruzi RBP42 is expressed in all life cycle stages of the parasite as determined by immunoblot and immunofluorescence microscopy. In each case, the protein is localized to the cytoplasm, indicating a role for T. cruzi RBP42 in post-transcriptional activities in all stages of the parasite life cycle. We speculate that RBP42 influences the dynamic metabolic pathways responsible for parasite infection and transmission.
KW - Chagas disease
KW - Immunofluorescence
KW - Transgenic parasites
KW - Trypanosoma cruzi
KW - Trypanosomes
KW - mRNA-binding proteins
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U2 - 10.1007/s00436-018-5787-9
DO - 10.1007/s00436-018-5787-9
M3 - Article
C2 - 29473141
AN - SCOPUS:85042380777
SN - 0932-0113
VL - 117
SP - 1095
EP - 1104
JO - Parasitology research
JF - Parasitology research
IS - 4
ER -