IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v8y2017i1d10.1038_ncomms15737.html
   My bibliography  Save this article

The m6A pathway facilitates sex determination in Drosophila

Author

Listed:
  • Lijuan Kan

    (Sloan-Kettering Institute)

  • Anya V. Grozhik

    (Weill Medical College, Cornell University)

  • Jeffrey Vedanayagam

    (Sloan-Kettering Institute)

  • Deepak P. Patil

    (Weill Medical College, Cornell University)

  • Nan Pang

    (Sloan-Kettering Institute)

  • Kok-Seong Lim

    (Massachusetts Institute of Technology)

  • Yi-Chun Huang

    (Florida State University)

  • Brian Joseph

    (Sloan-Kettering Institute)

  • Ching-Jung Lin

    (Sloan-Kettering Institute)

  • Vladimir Despic

    (Sloan-Kettering Institute)

  • Jian Guo

    (Key Laboratory of Insect Developmental and Evolutionary Biology, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences
    University of Chinese Academy of Sciences)

  • Dong Yan

    (Key Laboratory of Insect Developmental and Evolutionary Biology, Institute of Plant Physiology and Ecology, Shanghai Institutes for Biological Sciences, Chinese Academy of Sciences)

  • Shu Kondo

    (Invertebrate Genetics Laboratory, National Institute of Genetics)

  • Wu-Min Deng

    (Florida State University)

  • Peter C. Dedon

    (Massachusetts Institute of Technology)

  • Samie R. Jaffrey

    (Weill Medical College, Cornell University)

  • Eric C. Lai

    (Sloan-Kettering Institute)

Abstract

The conserved modification N6-methyladenosine (m6A) modulates mRNA processing and activity. Here, we establish the Drosophila system to study the m6A pathway. We first apply miCLIP to map m6A across embryogenesis, characterize its m6A ‘writer’ complex, validate its YTH ‘readers’ CG6422 and YT521-B, and generate mutants in five m6A factors. While m6A factors with additional roles in splicing are lethal, m6A-specific mutants are viable but present certain developmental and behavioural defects. Notably, m6A facilitates the master female determinant Sxl, since multiple m6A components enhance female lethality in Sxl sensitized backgrounds. The m6A pathway regulates Sxl processing directly, since miCLIP data reveal Sxl as a major intronic m6A target, and female-specific Sxl splicing is compromised in multiple m6A pathway mutants. YT521-B is a dominant m6A effector for Sxl regulation, and YT521-B overexpression can induce female-specific Sxl splicing. Overall, our transcriptomic and genetic toolkit reveals in vivo biologic function for the Drosophila m6A pathway.

Suggested Citation

  • Lijuan Kan & Anya V. Grozhik & Jeffrey Vedanayagam & Deepak P. Patil & Nan Pang & Kok-Seong Lim & Yi-Chun Huang & Brian Joseph & Ching-Jung Lin & Vladimir Despic & Jian Guo & Dong Yan & Shu Kondo & Wu, 2017. "The m6A pathway facilitates sex determination in Drosophila," Nature Communications, Nature, vol. 8(1), pages 1-16, August.
  • Handle: RePEc:nat:natcom:v:8:y:2017:i:1:d:10.1038_ncomms15737
    DOI: 10.1038/ncomms15737
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms15737
    File Function: Abstract
    Download Restriction: no

    File URL: https://libkey.io/10.1038/ncomms15737?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
    ---><---

    Citations

    Citations are extracted by the CitEc Project, subscribe to its RSS feed for this item.
    as


    Cited by:

    1. Guoqiang Zhang & Yongru Xu & Xiaona Wang & Yuanxiang Zhu & Liangliang Wang & Wenxin Zhang & Yiru Wang & Yajie Gao & Xuna Wu & Ying Cheng & Qinmiao Sun & Dahua Chen, 2022. "Dynamic FMR1 granule phase switch instructed by m6A modification contributes to maternal RNA decay," Nature Communications, Nature, vol. 13(1), pages 1-16, December.

    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_ncomms15737. 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.