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, Sally A. Mackenzie

Research output: Contribution to journalArticlepeer-review

67 Scopus citations


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.

Original languageEnglish (US)
Article number6386
JournalNature communications
StatePublished - Feb 27 2015
Externally publishedYes

Bibliographical note

Funding Information:
We thank Mahnaz Akhavan and the UCLA BSCRC BioSequencing Core for high-throughput Illumina sequencing for bisulfite sequencing and the Indiana University Center for Genomics and Bioinformatics for assistance with genome sequencing. We thank Mei Chen, E. Omar Lozano and Stephen Luebker for technical support and Drs Jeffrey Mower and Michael Fromm for valuable discussions during the course of this work. We acknowledge the Division of Chemical Sciences, Geosciences and Biosciences, Office of Basic Energy Sciences of DOE (DE-FG02-10ER16189) for funding the physiological and phenotype studies, NSF (IOS IOS 1126935) for the epigenetic studies and the Bill and Melinda Gates Foundation (OPP1088661) for the support of methylome sequencing.

Publisher Copyright:
© 2015 Macmillan Publishers Limited. All rights reserved.


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