1. Chromosomes and Gene Expression
  2. Immunology and Inflammation
Download icon

Major transcriptional changes observed in the Fulani, an ethnic group less susceptible to malaria

  1. Jaclyn E Quin
  2. Ioana Bujila
  3. Mariama Chérif
  4. Guillaume S Sanou
  5. Ying Qu
  6. Manijeh Vafa Homann
  7. Anna Rolicka
  8. Sodiomon B Sirima
  9. Mary A O'Connell
  10. Andreas Lennartsson
  11. Marita Troye-Blomberg
  12. Issa Nebie
  13. Ann-Kristin Östlund Farrants  Is a corresponding author
  1. The Wenner-Gren Instiute, Stockholm University, Sweden
  2. Centre National de Recherche et de Formation sur le Paludisme, Burkina Faso
  3. Karolinksa Institute, Sweden
  4. Karolinska Institute, Sweden
  5. The Wenner-Gren Institute, Stockholm University, Sweden
  6. Central European Institute of Technology, Czech Republic
  7. The Wenner-Gren Institute, Stockholm Univerity, Sweden
Short Report
  • Cited 21
  • Views 1,917
  • Annotations
Cite this article as: eLife 2017;6:e29156 doi: 10.7554/eLife.29156

Abstract

The Fulani ethnic group has relatively better protection from Plasmodium falciparum malaria, as reflected by fewer symptomatic cases of malaria, lower infection rates, and lower parasite densities compared to sympatric ethnic groups<strong>.</strong> However, the basis for this lower susceptibility to malaria by the Fulani is unknown. We have performed a pilot study to examine global transcription and DNA methylation patterns in specific immune cell populations in the Fulani to elucidate the mechanisms that confer the lower susceptibility to P.falciparum malaria. When we compared uninfected and infected Fulani individuals, in contrast to uninfected and infected individuals from the sympatric ethnic group Mossi, we observed a key difference: a strong transcriptional response was only detected in the monocyte fraction of the Fulani, where over 1000 genes were significantly differentially expressed upon P.falciparum infection.

Data availability

The following data sets were generated

Article and author information

Author details

  1. Jaclyn E Quin

    Department of Molecular Biosciences, The Wenner-Gren Instiute, Stockholm University, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  2. Ioana Bujila

    Department of Molecular Biosciences, The Wenner-Gren Instiute, Stockholm University, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  3. Mariama Chérif

    Centre National de Recherche et de Formation sur le Paludisme, Ouagadougou, Burkina Faso
    Competing interests
    The authors declare that no competing interests exist.
  4. Guillaume S Sanou

    Centre National de Recherche et de Formation sur le Paludisme, Ouagadougou, Burkina Faso
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-0536-616X
  5. Ying Qu

    Department of Biosciences and Nutrition, Karolinksa Institute, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  6. Manijeh Vafa Homann

    Infectious Disease Unit, Department of Medicine, Karolinska Institute, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  7. Anna Rolicka

    Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  8. Sodiomon B Sirima

    Centre National de Recherche et de Formation sur le Paludisme, Ouagadougou, Burkina Faso
    Competing interests
    The authors declare that no competing interests exist.
  9. Mary A O'Connell

    Central European Institute of Technology, Brno, Czech Republic
    Competing interests
    The authors declare that no competing interests exist.
  10. Andreas Lennartsson

    Department of Biosciences and Nutrition, Karolinska Institute, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  11. Marita Troye-Blomberg

    Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm University, Stockholm, Sweden
    Competing interests
    The authors declare that no competing interests exist.
  12. Issa Nebie

    Centre National de Recherche et de Formation sur le Paludisme, Ouagadougou, Burkina Faso
    Competing interests
    The authors declare that no competing interests exist.
  13. Ann-Kristin Östlund Farrants

    Department of Molecular Biosciences, The Wenner-Gren Institute, Stockholm Univerity, Stockholm, Sweden
    For correspondence
    anki.ostlund@su.se
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-9225-3264

Funding

SciLife pilot grant, Stockholm University

  • Mary A O'Connell
  • Marita Troye-Blomberg
  • Ann-Kristin Östlund Farrants

BioMalPar European Network of Excellence (LSHP-CT-2004-503578)

  • Ioana Bujila
  • Marita Troye-Blomberg

European Communite's Seventh Network Programme (FP7/2007-2013 N 242095)

  • Marita Troye-Blomberg

Sven and Lilly Lawskis Fund

  • Jaclyn E Quin

The funders had no role in study design, data collection and interpretation, or the decision to submit the work for publication.

Ethics

Human subjects: The study protocol and the informed consent were approved by the Institutional Review Board, The Technical Committee of the Centre National de Lutte contre le Paludisme of the Ministry of Health of Burkina Faso (2014/065/MS/SG/CNRFP/CIB). The study was conducted in compliance with International Conference on Harmonization's Good Clinical Practice principles, the Declaration of Helsinki, and the regulatory requirements of Burkina Faso.

Reviewing Editor

  1. Urszula Krzych, Walter Reed Army Institute of Research, United States

Publication history

  1. Received: May 31, 2017
  2. Accepted: September 5, 2017
  3. Accepted Manuscript published: September 19, 2017 (version 1)
  4. Version of Record published: October 5, 2017 (version 2)

Copyright

© 2017, Quin et al.

This article is distributed under the terms of the Creative Commons Attribution License permitting unrestricted use and redistribution provided that the original author and source are credited.

Metrics

  • 1,917
    Page views
  • 314
    Downloads
  • 21
    Citations

Article citation count generated by polling the highest count across the following sources: Crossref, Scopus, PubMed Central.

Download links

A two-part list of links to download the article, or parts of the article, in various formats.

Downloads (link to download the article as PDF)

Download citations (links to download the citations from this article in formats compatible with various reference manager tools)

Open citations (links to open the citations from this article in various online reference manager services)

Further reading

    1. Biochemistry and Chemical Biology
    2. Chromosomes and Gene Expression
    Fang Huang et al.
    Research Article

    The positive transcription elongation factor b (P-TEFb) is a critical co-activator for transcription of most cellular and viral genes, including those of HIV. While P-TEFb is regulated by 7SK snRNA in proliferating cells, P-TEFb is absent due to diminished levels of CycT1 in quiescent and terminally differentiated cells, which has remained unexplored. In these cells, we found that CycT1 not bound to CDK9 is rapidly degraded. Moreover, productive CycT1:CDK9 interactions are increased by PKC mediated phosphorylation of CycT1 in human cells. Conversely, dephosphorylation of CycT1 by PP1 reverses this process. Thus, PKC inhibitors or removal of PKC by chronic activation results in P-TEFb disassembly and CycT1 degradation. This finding not only recapitulates P-TEFb depletion in resting CD4+ T cells but also in anergic T cells. Importantly, our studies reveal mechanisms of P-TEFb inactivation underlying T cell quiescence, anergy, and exhaustion as well as proviral latency and terminally differentiated cells.

    1. Chromosomes and Gene Expression
    2. Computational and Systems Biology
    Lucy Ham et al.
    Research Article Updated

    Single-cell expression profiling opens up new vistas on cellular processes. Extensive cell-to-cell variability at the transcriptomic and proteomic level has been one of the stand-out observations. Because most experimental analyses are destructive we only have access to snapshot data of cellular states. This loss of temporal information presents significant challenges for inferring dynamics, as well as causes of cell-to-cell variability. In particular, we typically cannot separate dynamic variability from within cells (‘intrinsic noise’) from variability across the population (‘extrinsic noise’). Here, we make this non-identifiability mathematically precise, allowing us to identify new experimental set-ups that can assist in resolving this non-identifiability. We show that multiple generic reporters from the same biochemical pathways (e.g. mRNA and protein) can infer magnitudes of intrinsic and extrinsic transcriptional noise, identifying sources of heterogeneity. Stochastic simulations support our theory, and demonstrate that ‘pathway-reporters’ compare favourably to the well-known, but often difficult to implement, dual-reporter method.