Source Publication (e.g., journal title)

Plant Physiology

Document Type

Article

Publication Date

8-2015

DOI

10.1104/pp.15.00826

Abstract

Soybean cyst nematode (SCN, Heterodera glycines) induces the formation of a multinucleated feeding site, or syncytium, whose etiology includes massive gene expression changes. Nevertheless, the genetic networks underlying gene expression control in the syncytium are poorly understood. DNA methylation is a critical epigenetic mark that plays a key role in regulating gene expression. To determine the extent to which DNA methylation is altered in soybean roots during the susceptible interaction with SCN, we generated whole-genome cytosine methylation maps at single nucleotide resolution. The methylome analysis revealed that SCN induces hypo-methylation to a much higher extent than hyper-methylation. We identified 2,465 differentially hyper-methylated regions and 4,692 hypo-methylated regions in the infected roots compared with the non-infected control. In addition, a total number of 703 and 1346 unique genes were identified as overlapping with hyper- or hypo-methylated regions, respectively. The differential methylation in genes apparently occurs independently of gene size and GC content but exhibits strong preference for recently duplicated paralogs. Furthermore, a set of 278 genes was identified as specifically syncytium differentially methylated genes. Of these, we found genes associated with epigenetic regulation, phytohormone signaling, cell wall architecture, signal transduction and ubiquitination. This study provides new evidence that differential methylation is part of the regulatory mechanisms controlling gene expression changes in the nematode-induced syncytium, which seems to be heavily influenced by the traditional well-known transcription factor-based regulatory mechanisms.

Comments

This article was published openly thanks to the University of Tennessee Open Publishing Support Fund.

Copyright American Society of Plant Biologists, licensed under CC BY (Creative Commons Attribution).

Submission Type

Publisher's Version

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