The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status

Dongming Li, Ana Marie S. Palanca, So Youn Won, Lei Gao, Ying Feng, Ajay A. Vashisht, Li Liu, Yuanyuan Zhao, Xigang Liu, Xiuyun Wu, Shaofang Li, Brandon Le, Yun Ju Kim, Guodong Yang, Shengben Li, Jinyuan Liu, James A. Wohlschlegel, Hongwei Guo, Beixin Mo, Xuemei ChenJulie A. Law

Research output: Contribution to journalArticlepeer-review

12 Citations (Scopus)

Abstract

DNA methylation is associated with gene silencing in eukaryotic organisms. Although pathways controlling the establishment, maintenance and removal of DNA methylation are known, relatively little is understood about how DNA methylation influences gene expression. Here we identified a METHYL-CpG-BINDING DOMAIN 7 (MBD7) complex in Arabidopsis thaliana that suppresses the transcriptional silencing of two LUCIFERASE (LUC) reporters via a mechanism that is largely downstream of DNA methylation. Although mutations in components of the MBD7 complex resulted in modest increases in DNA methylation concomitant with decreased LUC expression, we found that these hyper-methylation and gene expression phenotypes can be genetically uncoupled. This finding, along with genome-wide profiling experiments showing minimal changes in DNA methylation upon disruption of the MBD7 complex, places the MBD7 complex amongst a small number of factors acting downstream of DNA methylation. This complex, however, is unique as it functions to suppress, rather than enforce, DNA methylation-mediated gene silencing.

Original languageEnglish
Article numbere19893
JournaleLife
Volume6
DOIs
Publication statusPublished - 2017 Apr 28

Bibliographical note

Publisher Copyright:
© Li et al.

All Science Journal Classification (ASJC) codes

  • Neuroscience(all)
  • Biochemistry, Genetics and Molecular Biology(all)
  • Immunology and Microbiology(all)

Fingerprint

Dive into the research topics of 'The MBD7 complex promotes expression of methylated transgenes without significantly altering their methylation status'. Together they form a unique fingerprint.

Cite this