近日來自中國科學院遺傳與發育生物學研究所的研究人員在組蛋白H3K4去甲基化酶研究中取得重要進展，證實水稻中的H3K4特異性去甲基酶JMJ703參與控制了轉座子活性，相關研究論文於1月14日在線發表在《美國科學院院刊》（PNAS）雜誌上。
領導這一研究的是中國科學院遺傳發育所基因組生物學研究中心主任曹曉風（Xiaofeng Cao）。其2008年曾獲得美國杜邦青年科學家獎，2011年獲得「中國青年女科學獎」。研究小組的主要科研方向為DNA及組蛋白甲基化和小分子RNA調控機理。
轉座子（Transposable elements）廣泛存在於植物基因組中，是核DNA的重要組成部分。大約40%的水稻基因組是由轉座子組成，其中許多都是反轉錄轉座子，包括14%的LTR和1%的非LTR反轉錄轉座子。儘管它們分布廣泛且非常豐富，然而，卻只有極少數的轉座子被發現發生了轉座，表明轉座子活性有可能受到了宿主基因組的嚴密調控，將與活性轉座相關的潛在誘變效應降到最低。
與這一概念相一致的是，越來越多的證據表明：如DNA甲基化、RNA幹擾和H3K9me2等表觀遺傳沉默信號，在轉錄和轉錄後水平上選擇性發揮功能，抑制了轉座子活性。然而目前仍不清楚，與活性轉錄相關的組蛋白修飾去除是否也參與了轉座子沉默。
在這篇文章中，研究人員證實水稻蛋白JMJ703，作為一種活性H3K4特異性去甲基酶，是轉座子沉默的必要條件。JMJ703活性受損可引起H3K4me3水平增高，導致大量的內源基因錯誤調控，兩個非LTR反轉錄轉座子家族轉座重激活。有趣的是，JMJ703缺失並不會影響從前發現的其他表觀遺傳信號沉默的轉座子。這些結果表明活性組蛋白修飾去除與轉座子沉默有關，不同的轉座子亞類有可能受到不同的表觀信號通路調控。
新研究揭示了組蛋白H3K4me3去甲基酶在高等植物反轉錄轉座子沉默中起重要作用。這項工作揭示了活性表觀遺傳標記去除與反轉錄轉座子沉默之間的聯繫，對於闡明人類的腫瘤發生機制也具有參考意義。(生物谷Bioon.com)
Control of transposon activity by a histone H3K4 demethylase in rice
Xiekui Cuia,b,1, Ping Jinc,d,1, Xia Cuia, Lianfeng Gua, Zhike Lua, Yongming Xuea,b, Liya Weia,b, Jianfei Qia, Xianwei Songa, Ming Luoe, Gynheung Anc, and Xiaofeng Caoa,2
Transposable elements (TEs) are ubiquitously present in plant genomes and often account for significant fractions of the nuclear DNA. For example, roughly 40% of the rice genome consists of TEs, many of which are retrotransposons, including 14% LTR- and ∼1% non-LTR retrotransposons. Despite their wide distribution and abundance, very few TEs have been found to be transpositional, indicating that TE activities may be tightly controlled by the host genome to minimize the potentially mutagenic effects associated with active transposition. Consistent with this notion, a growing body of evidence suggests that epigenetic silencing pathways such as DNA methylation, RNA interference, and H3K9me2 function collectively to repress TE activity at the transcriptional and posttranscriptional levels. It is not yet clear, however, whether the removal of histone modifications associated with active transcription is also involved in TE silencing. Here, we show that the rice protein JMJ703 is an active H3K4-specific demethylase required for TEs silencing. Impaired JMJ703 activity led to elevated levels of H3K4me3, the misregulation of numerous endogenous genes, and the transpositional reactivation of two families of non-LTR retrotransposons. Interestingly, loss of JMJ703 did not affect TEs (such as Tos17) previously found to be silenced by other epigenetic pathways. These results indicate that the removal of active histone modifications is involved in TE silencing and that different subsets of TEs may be regulated by distinct epigenetic pathways.