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Carril, O.

Publications and source records attributed to Carril, O..

2 recordsLinked to original sources

A high-throughput compound screen identifies multiple druggable targets in Plasmodium falciparum transmission stages

Most antimalarials are ineffective against the sexual transmission stages, known as gametocytes, of the malaria parasite Plasmodium falciparum. Their low sensitivity to drugs is attributed to limited compound uptake and a poorly understood form of cellular quiescence. Our current understanding of druggable transmission-blocking processes is therefore limited. Based on genetically engineered parasites that facilitate the mass production of synchronous mature gametocytes, we developed a high throughput drug screening platform that allowed us to test more than 50,000 compounds for gametocytocidal effects in one day. By screening a diversity-oriented library, we identified over 40 molecules that kill mature gametocytes in the low nanomolar range. Using resistance selection coupled to whole genome sequencing and drug-target interaction modelling, we followed up on three chemically tractable compounds that are also highly active against asexual parasites and prevent gametocyte transmission to mosquitoes. We show that the compound ONX-0914, a specific inhibitor of the {beta}5i/LMP7 subunit of human immunoproteasomes, targets the parasite proteasomal {beta}5 subunit. In contrast, the compounds CR-1-31-B and brusatol interfere with translation by targeting eukaryotic initiation factor 4A (eIF4A) and the peptidyl transferase center (PTC) of the 80S ribosome, respectively. Interestingly, parasite resistance to brusatol, a broad-spectrum antitumor drug, is linked to the differential modification of specific rRNA bases near the ribosomal A-site, mediated by altered base specificity of a rRNA methyltransferase. In summary, we successfully combined high-throughput compound screening with drug target deconvolution to reveal the targets and mode-of-action for three potent gametocytocidal molecules and discover the mechanism of resistance to the anti-tumorigenic drug brusatol. In addition to critically advancing our understanding of mature gametocyte biology and druggable processes in P. falciparum transmission stages, our observations made with brusatol-resistant parasites may become relevant for anti-cancer drug research.

molecular biology↗

A variant rRNA serves as a translational repressor in Plasmodium falciparum

Ribosome composition can vary through differences in associated proteins, post-transcriptional and post-translational modifications. Such heterogeneity enables ribosomes to respond to environmental1 or pathological2,3 conditions, and modulate localized translation4. A long-standing observation has also been the differential expression of variant ribosomal RNA (rRNA) alleles across developmental5-7 or cellular states8-14. Yet how exchanging the catalytic ribosome core could regulate translational outcomes remains unknown. Here, we report the functional characterization of a genomically-encoded, divergent rRNA that serves as a dominant-negative repressor of translation during host-to-vector transmission in the human malaria parasite. This allele only encodes for large subunit rRNAs, lacks ITS2 splicing, yet retains conserved rRNA modification and folding patterns alongside vast expansion segments. The resulting large subunit engages mRNA at translation start sites but appears to elongate inefficiently, likely due to divergences in the peptidyl transferase center obstructing the exit tunnel. Through its precisely timed transcription immediately after transmission, this rRNA represses mRNAs that were highly translated in the human, facilitating the transition of the translational program for mosquito-stage development. Our data identify a repressive ribosome population whose antagonistic function is encoded by an independently evolved, variant rRNA allele, defining the conceptual foundation for an additional layer of inherent translational regulation.

molecular biology↗