IDEAS home Printed from https://ideas.repec.org/a/nat/natcom/v7y2016i1d10.1038_ncomms11640.html
   My bibliography  Save this article

MTHFD1 controls DNA methylation in Arabidopsis

Author

Listed:
  • Martin Groth

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Guillaume Moissiard

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Markus Wirtz

    (Centre for Organismal Studies, University of Heidelberg)

  • Haifeng Wang

    (Basic Forestry and Proteomics Research Center, Haixia Institute of Science and Technology (HIST), Fujian Province Key Laboratory of Plant Virology, Institute of Plant Virology, Fujian Agriculture and Forestry University)

  • Carolina Garcia-Salinas

    (Tecnologico de Monterrey, Campus Monterrey)

  • Perla A. Ramos-Parra

    (Tecnologico de Monterrey, Campus Monterrey)

  • Sylvain Bischof

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Suhua Feng

    (Cell, and Developmental Biology, University of California Los Angeles
    Eli & Edythe Broad Center of Regenerative Medicine & Stem Cell Research, University of California Los Angeles
    Howard Hughes Medical Institute, University of California Los Angeles)

  • Shawn J. Cokus

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Amala John

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Danielle C. Smith

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Jixian Zhai

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Christopher J. Hale

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Jeff A. Long

    (Cell, and Developmental Biology, University of California Los Angeles)

  • Ruediger Hell

    (Centre for Organismal Studies, University of Heidelberg)

  • Rocío I. Díaz de la Garza

    (Tecnologico de Monterrey, Campus Monterrey)

  • Steven E. Jacobsen

    (Cell, and Developmental Biology, University of California Los Angeles
    Eli & Edythe Broad Center of Regenerative Medicine & Stem Cell Research, University of California Los Angeles
    Howard Hughes Medical Institute, University of California Los Angeles)

Abstract

DNA methylation is an epigenetic mechanism that has important functions in transcriptional silencing and is associated with repressive histone methylation (H3K9me). To further investigate silencing mechanisms, we screened a mutagenized Arabidopsis thaliana population for expression of SDCpro-GFP, redundantly controlled by DNA methyltransferases DRM2 and CMT3. Here, we identify the hypomorphic mutant mthfd1-1, carrying a mutation (R175Q) in the cytoplasmic bifunctional methylenetetrahydrofolate dehydrogenase/methenyltetrahydrofolate cyclohydrolase (MTHFD1). Decreased levels of oxidized tetrahydrofolates in mthfd1-1 and lethality of loss-of-function demonstrate the essential enzymatic role of MTHFD1 in Arabidopsis. Accumulation of homocysteine and S-adenosylhomocysteine, genome-wide DNA hypomethylation, loss of H3K9me and transposon derepression indicate that S-adenosylmethionine-dependent transmethylation is inhibited in mthfd1-1. Comparative analysis of DNA methylation revealed that the CMT3 and CMT2 pathways involving positive feedback with H3K9me are mostly affected. Our work highlights the sensitivity of epigenetic networks to one-carbon metabolism due to their common S-adenosylmethionine-dependent transmethylation and has implications for human MTHFD1-associated diseases.

Suggested Citation

  • Martin Groth & Guillaume Moissiard & Markus Wirtz & Haifeng Wang & Carolina Garcia-Salinas & Perla A. Ramos-Parra & Sylvain Bischof & Suhua Feng & Shawn J. Cokus & Amala John & Danielle C. Smith & Jix, 2016. "MTHFD1 controls DNA methylation in Arabidopsis," Nature Communications, Nature, vol. 7(1), pages 1-13, September.
    • Handle: RePEc:nat:natcom:v:7:y:2016:i:1:d:10.1038_ncomms11640
    DOI: 10.1038/ncomms11640
    as

    Download full text from publisher

    File URL: https://www.nature.com/articles/ncomms11640
    File Function: Abstract
    Download Restriction: no
    File URL: https://libkey.io/10.1038/ncomms11640?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:7:y:2016:i:1:d:10.1038_ncomms11640. 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.