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Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum
BACKGROUND: In eukaryotic organisms, gene expression is regulated at multiple levels during the processes of transcription and translation. The absence of a tight regulatory network for transcription in the human malaria parasite suggests that gene expression may largely be controlled at post-transc...
Autores principales: | , , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
BioMed Central
2013
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053746/ https://www.ncbi.nlm.nih.gov/pubmed/24267660 http://dx.doi.org/10.1186/gb-2013-14-11-r128 |
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author | Bunnik, Evelien M Chung, Duk-Won Doug Hamilton, Michael Ponts, Nadia Saraf, Anita Prudhomme, Jacques Florens, Laurence Le Roch, Karine G |
author_facet | Bunnik, Evelien M Chung, Duk-Won Doug Hamilton, Michael Ponts, Nadia Saraf, Anita Prudhomme, Jacques Florens, Laurence Le Roch, Karine G |
author_sort | Bunnik, Evelien M |
collection | PubMed |
description | BACKGROUND: In eukaryotic organisms, gene expression is regulated at multiple levels during the processes of transcription and translation. The absence of a tight regulatory network for transcription in the human malaria parasite suggests that gene expression may largely be controlled at post-transcriptional and translational levels. RESULTS: In this study, we compare steady-state mRNA and polysome-associated mRNA levels of Plasmodium falciparum at different time points during its asexual cell cycle. For more than 30% of its genes, we observe a delay in peak transcript abundance in the polysomal fraction as compared to the steady-state mRNA fraction, suggestive of strong translational control. Our data show that key regulatory mechanisms could include inhibitory activity of upstream open reading frames and translational repression of the major virulence gene family by intronic transcripts. In addition, we observe polysomal mRNA-specific alternative splicing events and widespread transcription of non-coding transcripts. CONCLUSIONS: These different layers of translational regulation are likely to contribute to a complex network that controls gene expression in this eukaryotic pathogen. Disrupting the mechanisms involved in such translational control could provide novel anti-malarial strategies. |
format | Online Article Text |
id | pubmed-4053746 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2013 |
publisher | BioMed Central |
record_format | MEDLINE/PubMed |
spelling | pubmed-40537462014-06-12 Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum Bunnik, Evelien M Chung, Duk-Won Doug Hamilton, Michael Ponts, Nadia Saraf, Anita Prudhomme, Jacques Florens, Laurence Le Roch, Karine G Genome Biol Research BACKGROUND: In eukaryotic organisms, gene expression is regulated at multiple levels during the processes of transcription and translation. The absence of a tight regulatory network for transcription in the human malaria parasite suggests that gene expression may largely be controlled at post-transcriptional and translational levels. RESULTS: In this study, we compare steady-state mRNA and polysome-associated mRNA levels of Plasmodium falciparum at different time points during its asexual cell cycle. For more than 30% of its genes, we observe a delay in peak transcript abundance in the polysomal fraction as compared to the steady-state mRNA fraction, suggestive of strong translational control. Our data show that key regulatory mechanisms could include inhibitory activity of upstream open reading frames and translational repression of the major virulence gene family by intronic transcripts. In addition, we observe polysomal mRNA-specific alternative splicing events and widespread transcription of non-coding transcripts. CONCLUSIONS: These different layers of translational regulation are likely to contribute to a complex network that controls gene expression in this eukaryotic pathogen. Disrupting the mechanisms involved in such translational control could provide novel anti-malarial strategies. BioMed Central 2013 2013-11-22 /pmc/articles/PMC4053746/ /pubmed/24267660 http://dx.doi.org/10.1186/gb-2013-14-11-r128 Text en Copyright © 2013 Bunnik et al.; licensee BioMed Central Ltd. http://creativecommons.org/licenses/by/2.0 This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited. The Creative Commons Public Domain Dedication waiver (http://creativecommons.org/publicdomain/zero/1.0/) applies to the data made available in this article, unless otherwise stated. |
spellingShingle | Research Bunnik, Evelien M Chung, Duk-Won Doug Hamilton, Michael Ponts, Nadia Saraf, Anita Prudhomme, Jacques Florens, Laurence Le Roch, Karine G Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title | Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title_full | Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title_fullStr | Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title_full_unstemmed | Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title_short | Polysome profiling reveals translational control of gene expression in the human malaria parasite Plasmodium falciparum |
title_sort | polysome profiling reveals translational control of gene expression in the human malaria parasite plasmodium falciparum |
topic | Research |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4053746/ https://www.ncbi.nlm.nih.gov/pubmed/24267660 http://dx.doi.org/10.1186/gb-2013-14-11-r128 |
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