1. Genetics and Genomics
  2. Plant Biology
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The genome and phenome of the green alga Chloroidium sp. UTEX 3007 reveal adaptive traits for desert acclimatization

Research Article
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Cite this article as: eLife 2017;6:e25783 doi: 10.7554/eLife.25783

Abstract

To investigate the phenomic and genomic traits that allow green algae to survive in deserts, we characterized a ubiquitous species, Chloroidium sp. UTEX 3007, which we isolated from multiple locations in the United Arab Emirates (UAE). Metabolomic analyses of Chloroidium sp. UTEX 3007 indicated that the alga accumulates a broad range of carbon sources, including several desiccation tolerance-promoting sugars and unusually large stores of palmitate. Growth assays revealed capacities to grow in salinities from zero to 60 g/L and to grow heterotrophically on >40 distinct carbon sources. Assembly and annotation of genomic reads yielded a 52.5 Mbp genome with 8153 functionally annotated genes. Comparison with other sequenced green algae revealed unique protein families involved in osmotic stress tolerance and saccharide metabolism that support phenomic studies. Our results reveal the robust and flexible biology utilized by a green alga to successfully inhabit a desert coastline.

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Article and author information

Author details

  1. David R Nelson

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    For correspondence
    drn2@nyu.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-8868-5734
  2. Basel Khraiwesh

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  3. Weiqi Fu

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-7368-383X
  4. Saleh Alseekh

    Max Planck Institute of Molecular Plant Physiology, Potsdam-Golm, Germany
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0003-2067-5235
  5. Ashish Kumar Jaiswal

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6193-1824
  6. Amphun Chaiboonchoe

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-0009-0806
  7. Khaled M Hazzouri

    Center for Genomics and Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  8. Matthew J O'Connor

    Core Technology Platform, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  9. Glenn L Butterfoss

    Center for Genomics and Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  10. Nizar Drou

    Center for Genomics and Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  11. Jillian D Rowe

    Center for Genomics and Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  12. Jamil Harb

    Max Planck Institute of Molecular Plant Physiology, Potsdam-Golm, Germany
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0001-6334-3746
  13. Alisdair R Fernie

    Max Planck Institute of Molecular Plant Physiology, Potsdam-Golm, Germany
    Competing interests
    The authors declare that no competing interests exist.
  14. Kristin C Gunsalus

    Center for Genomics and Systems Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    Competing interests
    The authors declare that no competing interests exist.
  15. Kourosh Salehi-Ashtiani

    Laboratory of Algal, Systems, and Synthetic Biology, New York University Abu Dhabi, Abu Dhabi, United Arab Emirates
    For correspondence
    ksa3@nyu.edu
    Competing interests
    The authors declare that no competing interests exist.
    ORCID icon "This ORCID iD identifies the author of this article:" 0000-0002-6521-5243

Funding

NYUAD Institute (Grant (G1205-1205i -1205h -1205e))

  • Kourosh Salehi-Ashtiani

NYUAD Faculty Research Funds

  • Kourosh Salehi-Ashtiani

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

Reviewing Editor

  1. Joerg Bohlmann, University of British Columbia, Canada

Publication history

  1. Received: February 5, 2017
  2. Accepted: June 15, 2017
  3. Accepted Manuscript published: June 17, 2017 (version 1)
  4. Version of Record published: July 13, 2017 (version 2)
  5. Version of Record updated: August 8, 2017 (version 3)

Copyright

© 2017, Nelson 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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  1. Further reading

Further reading

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    Background:

    Spinal muscular atrophy (SMA) is a neuromuscular disorder characterized by the degeneration of the second motor-neuron. The phenotype ranges from very severe to very mild forms. All patients have the homozygous loss of the SMN1 gene and a variable number of SMN2 (generally two-to-four copies), inversely related with the severity. The amazing results of the available treatments have made compelling the need of prognostic biomarkers to predict the progression trajectories of patients. Beside the SMN2 products, few other biomarkers have been evaluated so far, including some miRs.

    Methods:

    We performed whole miRNome analysis of muscle samples of patients and controls (14 biopsies and 9 cultures). The levels of muscle differentially expressed miRs were evaluated in serum samples (51 patients and 37 controls) and integrated with SMN2 copies, SMN2-full length transcript levels in blood and age (SMA-score).

    Results:

    Over 100 miRs were differentially expressed in SMA muscle; three of them (HSA-miR-181a-5p, -324-5p, -451a; SMA-miRs) were significantly up-regulated in serum of patients. The severity predicted by the SMA-score was related with that of the clinical classification at a correlation coefficient of 0.87 (p<10-5).

    Conclusions:

    miRNome analyses suggest the primary involvement of skeletal muscle in SMA pathogenesis; the SMA-miRs are likely actively released in the blood flow, even if their function and target cells require to be elucidated. The accuracy of the SMA-score needs to be verified in replicative studies: if confirmed, its use could be crucial for the routine prognostic assessment, also in pre-symptomatic patients.

    Funding:

    Telethon Italia (grant # GGP12116).

    1. Evolutionary Biology
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    Franziska Gruhl et al.
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