Epigenomic plasticity of Arabidopsis msh1 mutants under prolonged cold stress

Authors

Sunil Kumar Kenchanmane Raju, University of Nebraska-Lincoln
Mon-Ray Shao, University of Nebraska-LincolnFollow
Yashitola Wamboldt, University of Nebraska-Lincoln
Sally A. Mackenzie, The Pennsylvania State UniversityFollow

Date of this Version

2018

Citation

2018 The Authors. Plant Direct published by American Society of Plant Biologists, Society for Experimental Biology and John Wiley & Sons Ltd.

DOI: 10.1002/pld3.79

Comments

Plant Direct. 2018;1–12. wileyonlinelibrary.com/journal/pld3

Abstract

Dynamic transcriptional and epigenetic changes enable rapid adaptive benefit to environmental fluctuations. However, the underlying mechanisms and the extent to which this occurs are not well known. MutS Homolog 1 (MSH1) mutants cause heritable developmental phenotypes accompanied by modulation of defense, phytohormone, stress‐response, and circadian rhythm genes, as well as heritable changes in DNA methylation patterns. Consistent with gene expression changes, msh1 mutants display enhanced tolerance for abiotic stress including drought and salt stress, while showing increased susceptibility to freezing temperatures. Despite changes in defense and biotic stress‐response genes, msh1 mutants showed increasing susceptibility to the bacterial pathogen Pseudomonas syringae. Our results suggest that chronic cold and low light stress (10°C, 150 μmol m−2 s−1) influences non‐CG methylation to a greater degree in msh1 mutants compared to wild‐type Col‐0. Furthermore, CHG changes are more closely pericentromeric, whereas CHH changes are generally more dispersed. This increased variation in non‐CG methylation pattern does not significantly affect the msh1‐derived enhanced growth behavior after mutants are crossed with isogenic wild type, reiterating the importance of CG methylation changes in msh1‐derived enhanced vigor. These results indicate that msh1methylome is hyper‐responsive to environmental stress in a manner distinct from the wild‐type response, but CG methylation changes are potentially responsible for growth vigor changes in the crossed progeny.