首页> 美国卫生研究院文献>Plant Signaling Behavior >A functional Small Ubiquitin-like Modifier (SUMO) interacting motif (SIM) in the gibberellin hormone receptor GID1 is conserved in cereal crops and disrupting this motif does not abolish hormone dependency of the DELLA-GID1 interaction
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A functional Small Ubiquitin-like Modifier (SUMO) interacting motif (SIM) in the gibberellin hormone receptor GID1 is conserved in cereal crops and disrupting this motif does not abolish hormone dependency of the DELLA-GID1 interaction

机译:赤霉素类激素受体GID1中的功能性小泛素样修饰剂(SUMO)相互作用基序(SIM)在谷物作物中得以保存并且破坏该基序不会消除DELLA-GID1相互作用的激素依赖性

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摘要

Plants survive adversity by modulating their growth in response to changing environmental signals. The phytohormone Gibberellic acid (GA) plays a central role in regulating these adaptive responses by stimulating the degradation of growth repressing DELLA proteins which accumulate during stress. The current model for GA signaling describes how this hormone binds to its receptor GID1 so promoting association of GID1 with DELLA, which then undergoes ubiquitin-mediated proteasomal degradation. Recent data revealed that conjugation of DELLAs to the Small Ubiquitin-like Modifier (SUMO) protein enables plants to modulate its abundance during environmental stress. This is achieved by SUMOylated DELLAs sequestering GID1 via its SUMO interacting motif (SIM) allowing non-SUMOylated DELLAs to accumulate leading to growth restraint under stress and potential yield loss. We demonstrate that GID1 proteins across the major cereal crops contain a functional SIM able to bind SUMO1. Site directed mutagenesis and yeast 2 hybrid experiments reveal that it is possible to disrupt the SIM-SUMO interaction motif without affecting the GA dependent DELLA–GID1 interaction and thereby uncoupling SUMO–mediated inhibition from DELLA degradation. Arabidopsis plants overexpressing a SIM mutant allele of GID1 perform better at relieving DELLA restraint than wild–type GID1. This evidence suggests that manipulating the SIM motif in the GA receptor may provide a possible route to developing stress tolerant crops plants.
机译:植物通过适应不断变化的环境信号调节其生长,从而在逆境中生存。植物激素赤霉素(GA)通过刺激在压力下积累的抑制生长的DELLA蛋白降解来调节这些适应性反应。当前的GA信号传导模型描述了该激素如何与其受体GID1结合,从而促进GID1与DELLA的缔合,然后DELLA受到泛素介导的蛋白酶体降解。最近的数据显示,DELLAs与小泛素样修饰剂(SUMO)蛋白结合可以使植物在环境胁迫期间调节其丰度。这是通过SUMO酰化的DELLA通过其SUMO相互作用基序(SIM)隔离GID1来实现的,SIMID使非SUMO酰化的DELLA积累,导致在胁迫和潜在产量损失下的生长受到限制。我们证明了主要谷物作物上的GID1蛋白均含有能够结合SUMO1的功能性SIM。定点诱变和酵母2杂交实验表明,有可能破坏SIM-SUMO相互作用基序而不影响GA依赖的DELLA-GID1相互作用,从而使SUMO介导的抑制与DELLA降解脱钩。过量表达GID1的SIM突变等位基因的拟南芥植物在缓解DELLA抑制方面比野生型GID1表现更好。该证据表明,操纵GA受体中的SIM基序可能为发展耐逆性农作物提供一条可能的途径。

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