J Integr Plant Biol. ›› 2019, Vol. 61 ›› Issue (12): 1243-1254.DOI: 10.1111/jipb.12787

• Plant Reproduction Biology • Previous Articles     Next Articles

EXPORTIN 1A prevents transgene silencing in Arabidopsis by modulating nucleo-cytoplasmic partitioning of HDA6

Guohui Zhu1,2, Yanan Chang3,4, Xuezhong Xu2, Kai Tang1,3, Chunxiang Chen3,4, Mingguang Lei3, Jian-Kang Zhu1,3*and Cheng-Guo Duan1,3*   

  1. 1Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, IN 47907, USA
    2College of Life Sciences, South China Agricultural University, Guangzhou 510642, China
    3Shanghai Center for Plant Stress Biology and Center of Excellence for Molecular Plant Sciences, the Chinese Academy of Sciences, Shanghai 201602, China
    4The University of Chinese Academy of Sciences, Beijing 100049, China

    *Correspondences:
    Email: Jian-Kang Zhu (jkzhu@sibs.ac.cn); Cheng-Guo Duan (cgduan@sibs.ac.cn, Dr. Duan is fully responsible for the distributions of all materials associated with this article)
  • Received:2018-12-29 Accepted:2019-01-25 Online:2019-01-30 Published:2019-12-01

Abstract: In eukaryotic cells, transport of macromolecules across the nuclear envelope is an essential process that ensures rapid exchange of cellular components, including protein and RNA molecules. Chromatin regulators involved in epigenetic control are among the molecules exported across the nuclear envelope, but the significance of this nucleo‐cytoplasmic trafficking is not well understood. Here, we use a forward screen to isolate XPO1A (a nuclear export receptor in Arabidopsis) as an anti‐silencing factor that protects transgenes from transcriptional silencing. Loss‐of‐function of XPO1A leads to locus‐specific DNA hypermethylation at transgene promoters and some endogenous loci. We found that XPO1A directly interacts with histone deacetylase HDA6 in vivo and that the xpo1a mutation causes increased nuclear retention of HDA6 protein and results in reduced histone acetylation and enhanced transgene silencing. Our results reveal a new mechanism of epigenetic regulation through the modulation of XPO1A‐dependent nucleo‐cytoplasm partitioning of a chromatin regulator.

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