A reciprocal inhibition between ARID1 and MET1 in male and female gametes in Arabidopsis
A reciprocal inhibition between ARID1 and MET1 in male and female gametes in Arabidopsis
复制标题
拟南芥雄性和雌性配子中 ARID1 和 MET1 之间的相互抑制
DOI：
10.1111/jipb.12573
复制
发表时间：
2017-09-01
影响因子：
11.4
通讯作者：
Zheng, Binglian
中科院分区：
文献类型：
--
作者：
Li, Lei;Wu, Wenye;Zheng, Binglian
雌配子体和雄配子体都有伴细胞和配子。MET 1是一种DNA甲基转移酶，在伴随细胞中下调。然而，MET 1在配子体中的差异调节方式仍然未被探索。ARID1是一种在精子细胞中特异性缺失的转录因子，被MET 1依赖性CG甲基化占据。在这里，我们表明，MET1限制ARID1的雄性配子的营养细胞，但ARID1反过来抑制MET1在雌性配子的中央细胞。与野生型花粉中营养细胞定位相比，在met1突变体中ARID1扩展到精细胞。为了了解MET1依赖的ARID1抑制是否存在于雌性配子发生过程中，我们首先表明ARID1在大孢子母细胞（MMC）中表达，在成熟的中央细胞中检测到ARID1而不是MET1。有趣的是，与野生型胚珠的中央细胞和卵细胞中不存在MET 1相比，干旱型胚珠中MET 1在这两个细胞中显著积累。最后，我们表明，ARID1和MET 1都需要MMC的细胞规格。总的来说，我们的研究结果揭示了ARID1和MET 1之间的相互依赖性，并为进一步了解MMC的特异性可能受DNA甲基化的调控提供了线索。
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.