IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_s41467-017-01806-8.html
   My bibliography  Save this article

Mussel larvae modify calcifying fluid carbonate chemistry to promote calcification

Author

Listed:
  • Kirti Ramesh

    (GEOMAR Helmholtz Centre for Ocean Research Kiel)

  • Marian Y. Hu

    (Institute of Physiology, Christian-Albrechts-University Kiel)

  • Jörn Thomsen

    (GEOMAR Helmholtz Centre for Ocean Research Kiel)

  • Markus Bleich

    (Institute of Physiology, Christian-Albrechts-University Kiel)

  • Frank Melzner

    (GEOMAR Helmholtz Centre for Ocean Research Kiel)

Abstract

Understanding mollusk calcification sensitivity to ocean acidification (OA) requires a better knowledge of calcification mechanisms. Especially in rapidly calcifying larval stages, mechanisms of shell formation are largely unexplored—yet these are the most vulnerable life stages. Here we find rapid generation of crystalline shell material in mussel larvae. We find no evidence for intracellular CaCO3 formation, indicating that mineral formation could be constrained to the calcifying space beneath the shell. Using microelectrodes we show that larvae can increase pH and [CO3 2−] beneath the growing shell, leading to a ~1.5-fold elevation in calcium carbonate saturation state (Ωarag). Larvae exposed to OA exhibit a drop in pH, [CO3 2−] and Ωarag at the site of calcification, which correlates with decreased shell growth, and, eventually, shell dissolution. Our findings help explain why bivalve larvae can form shells under moderate acidification scenarios and provide a direct link between ocean carbonate chemistry and larval calcification rate.

Suggested Citation

  • Kirti Ramesh & Marian Y. Hu & Jörn Thomsen & Markus Bleich & Frank Melzner, 2017. "Mussel larvae modify calcifying fluid carbonate chemistry to promote calcification," Nature Communications, Nature, vol. 8(1), pages 1-8, December.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01806-8
    DOI: 10.1038/s41467-017-01806-8
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-017-01806-8
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/s41467-017-01806-8?utm_source=ideas
    LibKey link: if access is restricted and if your library uses this service, LibKey will redirect you to where you can use your library subscription to access this item
    ---><---

    More about this item

    Statistics

    Access and download statistics

    Corrections

    All material on this site has been provided by the respective publishers and authors. You can help correct errors and omissions. When requesting a correction, please mention this item's handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_s41467-017-01806-8. See general information about how to correct material in RePEc.

    If you have authored this item and are not yet registered with RePEc, we encourage you to do it here. This allows to link your profile to this item. It also allows you to accept potential citations to this item that we are uncertain about.

    We have no bibliographic references for this item. You can help adding them by using this form .

    If you know of missing items citing this one, you can help us creating those links by adding the relevant references in the same way as above, for each refering item. If you are a registered author of this item, you may also want to check the "citations" tab in your RePEc Author Service profile, as there may be some citations waiting for confirmation.

    For technical questions regarding this item, or to correct its authors, title, abstract, bibliographic or download information, contact: Sonal Shukla or Springer Nature Abstracting and Indexing (email available below). General contact details of provider: http://www.nature.com .

    Please note that corrections may take a couple of weeks to filter through the various RePEc services.

    IDEAS is a RePEc service. RePEc uses bibliographic data supplied by the respective publishers.