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Adenosine methylation in Arabidopsis mRNA is associated with the 3? end and reduced levels cause developmental defects

Bodi, Zsuzsanna; Zhong, Silin; Mehra, Surbhi; Song, Jie; Graham, Neil; Li, Hongying; May, Sean; Fray, Rupert George


Zsuzsanna Bodi

Silin Zhong

Surbhi Mehra

Jie Song

Senior Research Fellow

Hongying Li

Rupert George Fray


We previously showed that the N6-methyladenosine (m6A) mRNA methylase is essential during Arabidopsis thaliana embryonic development. We also demonstrated that this modification is present at varying levels in all mature tissues. However, the requirement for the m6A in the mature plant was not tested. Here we show that a 90% reduction in m6A levels during later growth stages gives rise to plants with altered growth patterns and reduced apical dominance. The flowers of these plants commonly show defects in their floral organ number, size, and identity. The global analysis of gene expression from reduced m6A plants show that a significant number of down-regulated genes are involved in transport, or targeted transport, and most of the up-regulated genes are involved in stress and stimulus response processes. An analysis of m6A distribution in fragmented mRNA suggests that the m6A is predominantly positioned toward the 3′ end of transcripts in a region 100–150 bp before the poly(A) tail. In addition to the analysis of the phenotypic changes in the low methylation Arabidopsis plants we will review the latest advances in the field of mRNA internal methylation


Bodi, Z., Zhong, S., Mehra, S., Song, J., Graham, N., Li, H., …Fray, R. G. (2012). Adenosine methylation in Arabidopsis mRNA is associated with the 3′ end and reduced levels cause developmental defects. Frontiers in Plant Science, 3(48), Article 48.

Journal Article Type Article
Publication Date Mar 23, 2012
Deposit Date Mar 31, 2014
Publicly Available Date Mar 31, 2014
Journal Frontiers in Plant Science
Electronic ISSN 1664-462X
Publisher Frontiers Media
Peer Reviewed Peer Reviewed
Volume 3
Issue 48
Article Number 48
Public URL
Publisher URL


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