Arabidopsis MSH1 mutation alters the epigenome and produces heritable changes in plant growth

Kamaldeep S. Virdi, John D. Laurie, Ying-Zhi Xu, Jiantao Yu, Mon-Ray Shao, Robersy Sanchez, Hardik Kundariya, Dong Wang, Jean-Jack M. Riethoven, Yashitola Wamboldt, Maria P. Arrieta-Montiel, Vikas Shedge and Sally A. Mackenzie ()
Additional contact information
Kamaldeep S. Virdi: School of Biological Sciences, University of Nebraska
John D. Laurie: University of Nebraska
Ying-Zhi Xu: University of Nebraska
Jiantao Yu: University of Nebraska
Mon-Ray Shao: University of Nebraska
Robersy Sanchez: University of Nebraska
Hardik Kundariya: University of Nebraska
Dong Wang: University of Nebraska
Jean-Jack M. Riethoven: Center for Biotechnology, University of Nebraska
Yashitola Wamboldt: University of Nebraska
Maria P. Arrieta-Montiel: University of Nebraska
Vikas Shedge: University of Nebraska
Sally A. Mackenzie: University of Nebraska

Nature Communications, 2015, vol. 6, issue 1, 1-9

Abstract: Abstract Plant phenotypes respond to environmental change, an adaptive capacity that is at least partly transgenerational. However, epigenetic components of this interplay are difficult to measure. Depletion of the nuclear-encoded protein MSH1 causes dramatic and heritable changes in plant development, and here we show that crossing these altered plants with isogenic wild type produces epi-lines with heritable, enhanced growth vigour. Pericentromeric DNA hypermethylation occurs in a subset of msh1 mutants, indicative of heightened transposon repression, while enhanced growth epi-lines show large chromosomal segments of differential CG methylation, reflecting genome-wide reprogramming. When seedlings are treated with 5-azacytidine, root growth of epi-lines is restored to wild-type levels, implicating hypermethylation in enhanced growth. Grafts of wild-type floral stems to mutant rosettes produce progeny with enhanced growth and altered CG methylation strikingly similar to epi-lines, indicating a mobile signal when MSH1 is downregulated, and confirming the programmed nature of methylome and phenotype changes.

Date: 2015
References: Add references at CitEc
Citations:

Downloads: (external link)
https://www.nature.com/articles/ncomms7386 Abstract (text/html)

Related works:
This item may be available elsewhere in EconPapers: Search for items with the same title.

Export reference: BibTeX RIS (EndNote, ProCite, RefMan) HTML/Text

Persistent link: https://EconPapers.repec.org/RePEc:nat:natcom:v:6:y:2015:i:1:d:10.1038_ncomms7386

Ordering information: This journal article can be ordered from
https://www.nature.com/ncomms/

DOI: 10.1038/ncomms7386

Access Statistics for this article

Nature Communications is currently edited by Nathalie Le Bot, Enda Bergin and Fiona Gillespie

More articles in Nature Communications from Nature
Bibliographic data for series maintained by Sonal Shukla () and Springer Nature Abstracting and Indexing ().