1. Epidemiology and Global Health
  2. Genetics and Genomics
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Isolation and transcriptomic analysis of Anopheles gambiae oenocytes enables the delineation of hydrocarbon biosynthesis

  1. Linda Grigoraki  Is a corresponding author
  2. Xavier Grau-Bové
  3. Henrietta Carrington Yates
  4. Gareth J Lycett
  5. Hilary Ranson  Is a corresponding author
  1. Liverpool School of Tropical Medicine, United Kingdom
Research Article
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Cite this article as: eLife 2020;9:e58019 doi: 10.7554/eLife.58019

Abstract

The surface of insects is coated in cuticular hydrocarbons (CHCs); variations in the composition of this layer affect a range of traits including adaptation to arid environments and defence against pathogens and toxins. In the African malaria vector, Anopheles gambiae quantitative and qualitative variance in CHC composition have been associated with speciation, ecological habitat and insecticide resistance. Understanding how these modifications arise will inform us of how mosquitoes are responding to climate change and vector control interventions. CHCs are synthesised in sub-epidermal cells called oenocytes that are very difficult to isolate from surrounding tissues. Here we utilise a transgenic line with fluorescent oenocytes to purify these cells for the first time. Comparative transcriptomics revealed the enrichment of biological processes related to long chain fatty acyl-CoA biosynthesis and elongation of mono-, poly-unsaturated and saturated fatty acids and enabled us to delineate, and partially validate, the hydrocarbon biosynthetic pathway in An. gambiae.

Data availability

Transcriptome sequencing has been deposited in the European Nucleotide Archive (ENA), under PRJEB37240 project.All data generated or analysed during this study are included in the manuscript and supporting files. Source data files have been provided for Figures 1,2,3 and 5.

Article and author information

Author details

  1. Linda Grigoraki

    Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom
    For correspondence
    Linta.Grigoraki@lstmed.ac.uk
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8997-0406
  2. Xavier Grau-Bové

    Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-1978-5824
  3. Henrietta Carrington Yates

    Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-6199-7009
  4. Gareth J Lycett

    Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom
    Competing interests
    The authors declare that no competing interests exist.
  5. Hilary Ranson

    Vector Biology, Liverpool School of Tropical Medicine, Liverpool, United Kingdom
    For correspondence
    hilary.ranson@lstmed.ac.uk
    Competing interests
    The authors declare that no competing interests exist.

Funding

Wellcome (Sir Henry Wellcome Postdoctoral Fellowship,215894/Z/19/Z)

  • Linda Grigoraki

Liverpool School of Tropical Medicine (Director's Catalyst Fund)

  • Linda Grigoraki

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

Reviewing Editor

  1. Malcolm J McConville, The University of Melbourne, Australia

Publication history

  1. Received: April 17, 2020
  2. Accepted: June 12, 2020
  3. Accepted Manuscript published: June 15, 2020 (version 1)
  4. Version of Record published: July 10, 2020 (version 2)

Copyright

© 2020, Grigoraki 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.

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Further reading

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    Background: Identifying environmentally responsive genetic loci where DNA methylation is associated with coronary heart disease (CHD) may reveal novel pathways or therapeutic targets for CHD. We conducted the first prospective epigenome-wide analysis of DNA methylation in relation to incident CHD in the Asian population.

    Methods: We did a nested case-control study comprising incident CHD cases and 1:1 matched controls who were identified from the 10-year follow-up of the China Kadoorie Biobank. Methylation level of baseline blood leukocyte DNA was measured by Infinium Methylation EPIC BeadChip. We performed the single cytosine-phosphate-guanine (CpG) site association analysis and network approach to identify CHD-associated CpG sites and co-methylation gene module.

    Results: After quality control, 982 participants (mean age 50.1 years) were retained. Methylation level at 25 CpG sites across the genome was associated with incident CHD (genome-wide false discovery rate [FDR] < 0.05 or module-specific FDR <0.01). One SD increase in methylation level of identified CpGs was associated with differences in CHD risk, ranging from a 47% decrease to a 118% increase. Mediation analyses revealed 28.5% of the excessed CHD risk associated with smoking was mediated by methylation level at the promoter region of ANKS1A gene (P for mediation effect = 0.036). Methylation level at the promoter region of SNX30 was associated with blood pressure and subsequent risk of CHD, with the mediating proportion to be 7.7% (P = 0.003) via systolic blood pressure and 6.4% (P = 0.006) via diastolic blood pressure. Network analysis revealed a co-methylation module associated with CHD.

    Conclusions: We identified novel blood methylation alterations associated with incident CHD in the Asian population and provided evidence of the possible role of epigenetic regulations in the smoking- and BP-related pathways to CHD risk.

    Funding: This work was supported by National Natural Science Foundation of China (81390544 and 91846303). The CKB baseline survey and the first re-survey were supported by a grant from the Kadoorie Charitable Foundation in Hong Kong. The long-term follow-up is supported by grants from the UK Wellcome Trust (202922/Z/16/Z, 088158/Z/09/Z, 104085/Z/14/Z), grant (2016YFC0900500, 2016YFC0900501, 2016YFC0900504, 2016YFC1303904) from the National Key and Program of China, and Chinese Ministry of Science and Technology (2011BAI09B01).