J Integr Plant Biol ›› 2017, Vol. 59 ›› Issue (9): 657-668.DOI: 10.1111/jipb.12573

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A reciprocal inhibition between ARID1 and MET1 in male and female gametes in Arabidopsis

Lei Li, Wenye Wu, Youshang Zhao and Binglian Zheng*   

  • 收稿日期:2017-07-06 接受日期:2017-08-04 出版日期:2017-08-07 发布日期:2017-08-07

A reciprocal inhibition between ARID1 and MET1 in male and female gametes in Arabidopsis

Lei Li, Wenye Wu, Youshang Zhao and Binglian Zheng*   

  1. State Key Laboratory of Genetic Engineering, Collaborative Innovation Center for Genetics and Development, School of Life Sciences, Fudan University, Shanghai 200438, China
  • Received:2017-07-06 Accepted:2017-08-04 Online:2017-08-07 Published:2017-08-07
  • About author:*Correspondences: E-mail: Binglian Zheng (zhengbl@fudan.edu.cn)

摘要: DNA methylation is usually down-regulated in companion cells of plant gametes, in which either DNA methytransferases are repressed and/or DNA demethylases are locally increased. This work identified an Arabidopsis transcription factor ARID1 (AT-Rich Interacting Domain 1), which reciprocally regulates MET1, a major CG DNA methyltransferase, during plant gametophyte development.

Abstract:

Both female and male gametophytes harbor companion cells and gametes. MET1, a DNA methyltransferase, is down-regulated in companion cells. However, how MET1 is differentially regulated in gametophytes remains unexplored. ARID1, a transcription factor that is specifically depleted in sperm cells, is occupied by MET1-dependent CG methylation. Here, we show that MET1 confines ARID1 to the vegetative cell of male gametes, but ARID1 conversely represses MET1 in the central cell of female gametes. Compared to the vegetative cell-localization in wild type pollen, ARID1 expands to sperm cells in the met1 mutant. To understand whether MET1-dependent ARID1 inhibition exists during female gametogenesis, we first show that ARID1 is expressed in the megaspore mother cell (MMC), ARID1 but not MET1 is detectable in the central cell at maturity. Interestingly, compared to the absence of MET1 in the central cell and the egg cell of wild type ovules, MET1 significantly accumulates in these two cells in arid1 ovules. Lastly, we show that both ARID1 and MET1 are required for the cell specification of MMC. Collectively, our results uncover a reciprocal dependence between ARID1 and MET1, and provide a clue to further understand how the specification of MMC is likely regulated by DNA methylation.

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