IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v15y2024i1d10.1038_s41467-024-45195-1.html
   My bibliography  Save this article

Hormonal steroids induce multidrug resistance and stress response genes in Neisseria gonorrhoeae by binding to MtrR

Author

Listed:
  • Grace M. Hooks

    (Duke University School of Medicine)

  • Julio C. Ayala

    (Emory University School of Medicine
    Centers for Disease Control and Prevention)

  • Concerta L. Holley

    (Emory University School of Medicine)

  • Vijaya Dhulipala

    (Emory University School of Medicine)

  • Grace A. Beggs

    (Princeton University)

  • John R. Perfect

    (Duke University Medical Center)

  • Maria A. Schumacher

    (Duke University School of Medicine)

  • William M. Shafer

    (Emory University School of Medicine
    Veterans Affairs Medical Center
    Emory University School of Medicine)

  • Richard G. Brennan

    (Duke University School of Medicine)

Abstract

Transcriptional regulator MtrR inhibits the expression of the multidrug efflux pump operon mtrCDE in the pathogenic bacterium Neisseria gonorrhoeae. Here, we show that MtrR binds the hormonal steroids progesterone, β-estradiol, and testosterone, which are present at urogenital infection sites, as well as ethinyl estrogen, a component of some hormonal contraceptives. Steroid binding leads to the decreased affinity of MtrR for cognate DNA, increased mtrCDE expression, and enhanced antimicrobial resistance. Furthermore, we solve crystal structures of MtrR bound to each steroid, thus revealing their binding mechanisms and the conformational changes that induce MtrR.

Suggested Citation

  • Grace M. Hooks & Julio C. Ayala & Concerta L. Holley & Vijaya Dhulipala & Grace A. Beggs & John R. Perfect & Maria A. Schumacher & William M. Shafer & Richard G. Brennan, 2024. "Hormonal steroids induce multidrug resistance and stress response genes in Neisseria gonorrhoeae by binding to MtrR," Nature Communications, Nature, vol. 15(1), pages 1-14, December.
    • Handle: RePEc:nat:natcom:v:15:y:2024:i:1:d:10.1038_s41467-024-45195-1
    DOI: 10.1038/s41467-024-45195-1
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/s41467-024-45195-1
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/s41467-024-45195-1?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:15:y:2024:i:1:d:10.1038_s41467-024-45195-1. 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.