图1 植物中赤霉素的生物合成途径示意图 2ox：GA 2-氧化酶;3ox：GA 3-氧化酶;13ox：GA 13-氧化酶;20ox：GA 20-氧化酶;GGPP：牻牛儿基牻牛儿基焦磷酸;CPS：ent-copalyl二磷酸合酶;KS：ent-kaurene合酶;KO：ent-Kaurene氧化酶;KAO：ent-kaurenoic酸氧化酶。此图修改自Yamaguchi[2]

Fig. 1 Gibberellin biosynthesis pathways in plants 2ox：GA 2-oxidase. 3ox：GA 3-oxidase. 13ox：GA 13-oxidase. 20ox：GA 20-oxidase. GGDP：geranylgeranyl diphosphate. CPS：ent-copalyl diphosphate synthase. KS：ent-kaurene synthase. KO：ent-kaurene oxidase. KAO：ent-kaurenoic acid oxidase. This figure was modified from Yamaguchi[2]

图2 GA-GID1-DELLA信号传导途径示意图 GID1与生物活性的GA结合会导致其构象发生变化,从而促进与DELLA蛋白的相互作用。F-box蛋白的募集启动了SCF E3泛素连接酶介导的DELLA的泛素化,泛素化后的DELLA会进一步的被蛋白酶降解。DELLA的缺失减轻了其对生长抑制并抑制了其他DELLA介导的反应

Fig. 2 Sketch of GA-GID1-DELLAsignal transduction Binding with a bioactive GA results in a conformational change in the GID1 receptor,thus which promotes interaction with DELLA proteins. Recruitment of an F-box protein initiates ubiquitination of DELLA mediated by an SCF E3 ubiquitin ligase targeting the DELLA for proteasomal degradation. Deficiency of DELLA eliminates its growth repression and suppresses other DELLA-mediated reactions

图3 赤霉素合成和信号传导途径中的“绿色革命”基因 a：sd1等位基因的突变位点。sd1突变影响了GA20ox的活性。该酶负责催化GA53转化为GA20,生成生物活性产物GA1。GA20ox由3个外显子和2个内含子组成。每个突变分别用箭头（替换）或横线（缺失）来表示;b：GA是可导致生长抑制蛋白Rht的降解。突变型的Rht（Rht-B1b和Rht-D1b）对GAs诱导的降解不敏感。箭头表示Rht-B1b和Rht-D1b中终止密码的位置。C末端（浅蓝色）在所有相关蛋白中高度保守,并含有抑制因子活性。N端（绿色）是GAs信号识别域,包括2个GAs诱导降解所必需的高度保守的序列（深蓝色）。此图修改自Hedden等[6]和Sasaki等[9]3 水稻“绿色革命”基因semidwarf-1（sd-1）

Fig.3 Green Revolution genes in gibberellin biosynthesis and signal transduction a：Mutation sites of the sd1 alleles. sd1 mutations affect the activity of GA20ox,which catalyzes the conversion of GA53 to GA20 in the biosynthetic pathway to the biological active product,GA1. The GA20ox gene consists of three exons and two introns. The mutation in each allele is indicated by either an arrow（single-nucleotide substitution）or a line（internal deletion）. b：GA action results in the degradation of Rht. The mutant forms of Rht（Rht-B1b and Rht-D1b）are not susceptible to GA-induced degradation. The arrow indicates the position of terminal codons in Rht-B1b and Rht-D1b. The C-terminus（light blue）is highly conserved in all related proteins and contains the repressor activity. The N-terminus（green）contains the GA-signalling domain that includes two highly conserved motifs（dark blue）that are required for GA-induced degradation. This figure was modified from Hedden et al[6]and Sasaki et al[9]

图4 GRF4提高水稻中碳氮代谢效率 a：现有“绿色革命”品种（Green Revolution varieties,GRVs）中,DELLA类蛋白SLR1（SLENDER RICE1）会抑制OsGIF1和OsGRF4的相互作用,影响碳氮代谢;b：改良后的GRVs中,OsGRF4表达量的增加克服了SLR1对OsGIF1和OsGRF4相互作用的抑制,而且OsGRF4通过自激活效应有效的提高了碳氮代谢效率,促进了产量的提升。此图修改自Wang等[60]

Fig. 4 GRF4 increases the efficiency of nitrogen and carbon metabolism in rice a：In Green Revolution varieties（GRVs）,DELLA-like protein SLR1（SLENDER RICE1）inhibits the interaction between OsGIF1 and OsGRF4,which affects the metabolism of nitrogen（N）and carbon（C）. b：In improved GRVs,increased expressions of OsGRF4 overcomes the inhibition of SLR1 to OsGIF1-OsGRF4 interactions. In addition,OsGRF4 efficiently promotes nitrogen and carbon use efficiency by self-promotion and thus resulting in higher yields. This figure was modified from Wang et al[60]

图5 NGR5基因影响水稻分蘖数量的调控机理 水稻转录因子NGR5促进氮依赖的PRC2募集,进而阻断抑制分蘖基因的表达,促进分蘖。NGR5与赤霉素受体GID1结合后可被降解,而DELLA的积累可竞争性地与GA-GID1结合,抑制GID1-NGR5的相互作用,从而稳定NGR5。此图修改自Wu等[59]5 赤霉素代谢调控与“绿色革命”品种的广适性

Fig. 5 Mechanism of NGR5 regulating rice tillering The rice transcription factor NGR5 facilitates nitrogen-dependent recruitment of PRC2 to repress expression of tillering genes,thus promoting tillering in response to increasing nitrogen supply. NGR5 can be degraded after binding with the gibberellin receptor GID1,while DELLA accumulation inhibits the GID1-NGR5 interaction via competitively binding with GA-GID1,thus stabilizing. This figure was modified from Wu et al[59]

图6 赤霉素参与不同胁迫响应的示意图 不同的非生物胁迫会通过不同的效应因子诱导GA2oxs的表达,导致GAs合成的减少,进而促进DELLA的积累。在病原菌侵染条件下,茉莉酸（jasmonic acid,JA）介导的JAZ蛋白降解会解除其对DELLAs和MYC转录因子的抑制。MYC2同时也会促进DELLA的表达。DELLAs的积累通过抑制细胞伸长和分裂导致细胞停止生长;通过促进解毒酶编码基因表达抑制ROS产生;通过直接抑制JAZ活性促进JA应答。箭头和T条分别表示正调节和负调节。此图修改自Hedden等[1]

Fig.e 6 A simplified model for the role of GAs in stress response Different abiotic stresses induce the expression of GA2oxs via specific effectors,which results in the subsequent decrease of GAs synthesis,thus promotes DELLA accumulation. Under pathogen attack,JA-mediated JAZ protein degradation releases its repression to DELLAs and MYC transcription factors. MYC2 in turn also enhances the expression of DELLA. Accumulation of DELLAs leads to growth cessation via inhibition of cell elongation and cell division. Other protective mechanisms include the expression promotion of genes encoding detoxification enzymes to inhibit ROS generation,and promotion of JA response via direct repression of JAZ activity. Arrows and T-bars indicate positive or negative regulation,respectively. This figure was modified from Hedden et al[1]