Epigenetic controls of plant development and genome structure

FWA已被确定为负责晚开花表观遗传性状的基因（Mol Cell 6,791 -）。在本项目中，我们检测了FWA基因在正常发育过程中的表达。FWA基因在胚乳中以印迹方式特异表达。组织特异性和印迹FWA表达依赖于DNA甲基转移酶MET1和DNA去甲基化酶DEMETER （Science 303, 521-）。研究还表明，FT是开花的诱导剂（Science 309, 1052-）， FWA通过在蛋白质水平上抑制FT功能来影响开花（Plant Cell Physiol 48, 205-）。我们之前已经表明，拟南芥CACTA转座子在野生型中是沉默的，但它们在染色质重塑基因DDM1突变（DNA甲基化减少）中被动员（Nature 411, 212-）。在这个项目中，我们发现CACTA转座子在CG甲基化酶MET1和非CG甲基化酶CMT3的双突变体中转座。结果表明，DNA甲基化是固定这类转座子的必要条件（Curr Biol 13,421 -）。CACTA的转录被MET1或一个染色质组装因子FAS的突变去抑制（Curr Biol 13,421 -, Genes to Cells 18,153 -）。ddml突变破坏了CACTA位点或其他着中心点周围序列的异染色质，这种影响即使在野生型背景下也是可遗传的（EMBO J 21, 6549-）。利用该系统，我们还发现每个CACTA转位都不是针对异染色质的（遗传学168,961 -）。转座子如何积聚形成异染色质是很有趣的。

FWA has been identified as the gene responsible for a late-flowering epigenetic trait (Mol Cell 6, 791-). In this project, we examined expression of the FWA gene during normal development. The FWA gene was expressed specifically in endosperm in an imprinted manner. The tissue-specific and imprinted FWA expression depends on DNA methyltransferase MET1 and DNA demethylase DEMETER (Science 303, 521-). It was also shown that FT is the inducer of flowering (Science 309, 1052-), and the FWA affects flowering by inhibiting the FT function at the protein level (Plant Cell Physiol 48, 205-).We have previously shown that Arabidopsis CACTA transposons are silent in wild type, but they are mobilized in mutant of a chromatin remodeling gene DDM1 (decrease in DNA methylation) (Nature 411, 212-). In this project, we showed that the CACTA transposons transposed in the double mutants of CG methylase MET1 and non-CG methylase CMT3. The results suggest that DNA methylation is necessary for immobilization of this class of transposons (Curr Biol 13, 421-).Transcription of CACTA was de-repressed by mutations in the MET1 or a chromatin assembly factor FAS (Curr Biol 13, 421-, Genes to Cells 18, 153-). Heterochromatin in CACTA locus or other peri-centromeric sequences was disrupted by the ddml mutation, and this effect was heritable even in the wild type background (EMBO J 21, 6549-). Using this system, we also showed that each of CACTA transposition was not targeted to heterochromatin (Genetics 168, 961-). It is interesting how the transposons accumulate to form the heterochromatin.