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氮饥饿诱导拟南芥中转座元件的全基因组激活。

Nitrogen starvation induces genome-wide activation of transposable elements in Arabidopsis.

机构信息

State Key Laboratory of Protein and Plant Gene Research, School of Advanced Agricultural Sciences, Peking University, Beijing, 100871, China.

School of Life Sciences, Peking University, Beijing, 100871, China.

出版信息

J Integr Plant Biol. 2022 Dec;64(12):2374-2384. doi: 10.1111/jipb.13376. Epub 2022 Oct 21.

DOI:10.1111/jipb.13376
PMID:36178606
Abstract

Nitrogen (N) availability is a major limiting factor for plant growth and agricultural productivity. Although the gene regulation network in response to N starvation has been extensively studied, it remains unknown whether N starvation has an impact on the activity of transposable elements (TEs). Here, we report that TEs can be transcriptionally activated in Arabidopsis under N starvation conditions. Through genetic screening of idm1-14 suppressors, we cloned GLU1, which encodes a glutamate synthase that catalyzes the synthesis of glutamate in the primary N assimilation pathway. We found that glutamate synthase 1 (GLU1) and its functional homologs GLU2 and glutamate transport 1 (GLT1) are redundantly required for TE silencing, suggesting that N metabolism can regulate TE activity. Transcriptome and methylome analyses revealed that N starvation results in genome-wide TE activation without inducing obvious alteration of DNA methylation. Genetic analysis indicated that N starvation-induced TE activation is also independent of other well-established epigenetic mechanisms, including histone methylation and heterochromatin decondensation. Our results provide new insights into the regulation of TE activity under stressful environments in planta.

摘要

氮(N)供应是植物生长和农业生产力的主要限制因素。尽管已经广泛研究了响应 N 饥饿的基因调控网络,但仍不清楚 N 饥饿是否会影响转座元件(TE)的活性。在这里,我们报告在 N 饥饿条件下,拟南芥中的 TEs 可以被转录激活。通过 idm1-14 抑制子的遗传筛选,我们克隆了 GLU1,它编码谷氨酸合酶,该酶在初级 N 同化途径中催化谷氨酸的合成。我们发现谷氨酸合酶 1(GLU1)及其功能同源物 GLU2 和谷氨酸转运蛋白 1(GLT1)对于 TE 沉默是冗余的,这表明 N 代谢可以调节 TE 活性。转录组和甲基组分析表明,N 饥饿导致全基因组 TEs 激活,而不会引起 DNA 甲基化的明显改变。遗传分析表明,N 饥饿诱导的 TEs 激活也不依赖于其他已建立的表观遗传机制,包括组蛋白甲基化和异染色质去凝聚。我们的研究结果为植物在应激环境下调节 TE 活性提供了新的见解。

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