A variant rRNA serves as a translational repressor in Plasmodium falciparum
Abstract
Ribosome composition can vary through differences in associated proteins, post-transcriptional and post-translational modifications. Such heterogeneity enables ribosomes to respond to environmental 1 or pathological 2,3 conditions, and modulate localized translation 4 . A long-standing observation has also been the differential expression of variant ribosomal RNA (rRNA) alleles across developmental 5–7 or cellular states 8–14 . 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.
Related
- Plasmodium falciparum Myosin B is a slow motor optimized for force generation
- Substrate binding reorganizes the energetic landscape of Plasmodium falciparum hexose transporter PfHT1
- Nuclear acetyl-CoA production by acetyl-CoA synthetase enables dynamic histone acetylation and gene expression in Plasmodium falciparum
- Knob architecture and hemoglobin composition shape recovery dynamics of Plasmodium falciparum-infected erythrocytes
- Plasmodium falciparum putative Hsp90 functionally complements yeast Hsp90 and is inhibited in an isoform-specific manner
BibTeX
@misc{vignolini2026variant,
title = {{A variant rRNA serves as a translational repressor in Plasmodium falciparum}},
author = {Tiziano Vignolini and Olivia Carril and Victor Tobiasson and Joe Georgeson and Miguel Garcia-Campos and Justine Couble and Grégory Doré and Donna Matzov and Sebastian Hutchinson and Jessica Bryant and Moran Shalev-Benami and Schraga Schwartz and Sebastian Baumgarten},
howpublished = {HAL},
year = {2026},
month = jun,
doi = {10.64898/2026.06.17.732804},
url = {https://pasteur.hal.science/pasteur-05767228v1},
note = {CC BY-NC-ND 4.0},
}
RIS
TY - UNPB
TI - A variant rRNA serves as a translational repressor in Plasmodium falciparum
AU - Tiziano Vignolini
AU - Olivia Carril
AU - Victor Tobiasson
AU - Joe Georgeson
AU - Miguel Garcia-Campos
AU - Justine Couble
AU - Grégory Doré
AU - Donna Matzov
AU - Sebastian Hutchinson
AU - Jessica Bryant
AU - Moran Shalev-Benami
AU - Schraga Schwartz
AU - Sebastian Baumgarten
PY - 2026
DA - 2026/06/18
PB - HAL
DO - 10.64898/2026.06.17.732804
UR - https://pasteur.hal.science/pasteur-05767228v1
AB - Ribosome composition can vary through differences in associated proteins, post-transcriptional and post-translational modifications. Such heterogeneity enables ribosomes to respond to environmental 1 or pathological 2,3 conditions, and modulate localized translation 4 . A long-standing observation has also been the differential expression of variant ribosomal RNA (rRNA) alleles across developmental 5–7 or cellular states 8–14 . 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.
ER -