State Key Laboratory of Plant Cell and Chromosome Engineering, Institute of Genetics and Developmental Biology, Innovation Academy for Seed Design, Chinese Academy of Sciences, Beijing 100101, China.
College of Life Sciences, University of Chinese Academy of Sciences, Beijing 100049, China.
Science. 2020 Feb 7;367(6478). doi: 10.1126/science.aaz2046.
Because environmentally degrading inorganic fertilizer use underlies current worldwide cereal yields, future agricultural sustainability demands enhanced nitrogen use efficiency. We found that genome-wide promotion of histone H3 lysine 27 trimethylation (H3K27me3) enables nitrogen-induced stimulation of rice tillering: APETALA2-domain transcription factor NGR5 (NITROGEN-MEDIATED TILLER GROWTH RESPONSE 5) facilitates nitrogen-dependent recruitment of polycomb repressive complex 2 to repress branching-inhibitory genes via H3K27me3 modification. NGR5 is a target of gibberellin receptor GIBBERELLIN INSENSITIVE DWARF1 (GID1)-promoted proteasomal destruction. DELLA proteins (characterized by the presence of a conserved aspartate-glutamate-leucine-leucine-alanine motif) competitively inhibit the GID1-NGR5 interaction and explain increased tillering of green revolution varieties. Increased NGR5 activity consequently uncouples tillering from nitrogen regulation, boosting rice yield at low nitrogen fertilization levels. NGR5 thus enables enhanced nitrogen use efficiency for improved future agricultural sustainability and food security.
由于目前全球谷类作物的产量依赖于环境降解的无机肥料,因此未来农业的可持续性需要提高氮素利用效率。我们发现,组蛋白 H3 赖氨酸 27 三甲基化(H3K27me3)的全基因组促进作用使氮诱导的水稻分蘖得到刺激:APETALA2 结构域转录因子 NGR5(氮介导的分蘖生长响应 5)通过 H3K27me3 修饰促进多梳抑制复合物 2 对分支抑制基因的氮依赖性招募。NGR5 是赤霉素受体 GIBBERELLIN INSENSITIVE DWARF1(GID1)促进的蛋白体破坏的靶标。DELLA 蛋白(以存在保守的天冬氨酸-谷氨酸-亮氨酸-亮氨酸-丙氨酸基序为特征)竞争性抑制 GID1-NGR5 相互作用,并解释了绿色革命品种分蘖增加的现象。NGR5 活性的增加因此使分蘖与氮调节脱钩,在低氮施肥水平下提高了水稻产量。因此,NGR5 能够提高氮素利用效率,从而提高未来农业的可持续性和粮食安全。