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Release of the Repressive Activity of Rice DELLA Protein SLR1 by Gibberellin Does Not Require SLR1 Degradation in the gid2 Mutant[W]

机译:赤霉素释放水稻DELLA蛋白SLR1的抑制活性不需要在gid2突变体中降解SLR1 [W]

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摘要

The rice (Oryza sativa) DELLA protein SLR1 acts as a repressor of gibberellin (GA) signaling. GA perception by GID1 causes SLR1 protein degradation involving the F-box protein GID2; this triggers GA-associated responses such as shoot elongation and seed germination. In GA-insensitive and GA biosynthesis mutants, SLENDER RICE1 (SLR1) accumulates to high levels, and the severity of dwarfism is usually correlated with the level of SLR1 accumulation. An exception is the GA-insensitive F-box mutant gid2, which shows milder dwarfism than mutants such as gid1 and cps even though it accumulates higher levels of SLR1. The level of SLR1 protein in gid2 was decreased by loss of GID1 function or treatment with a GA biosynthesis inhibitor, and dwarfism was enhanced. Conversely, overproduction of GID1 or treatment with GA3 increased the SLR1 level in gid2 and reduced dwarfism. These results indicate that derepression of SLR1 repressive activity can be accomplished by GA and GID1 alone and does not require F-box (GID2) function. Evidence for GA signaling without GID2 was also provided by the expression behavior of GA-regulated genes such as GA-20oxidase1, GID1, and SLR1 in the gid2 mutant. Based on these observations, we propose a model for the release of GA suppression that does not require DELLA protein degradation.
机译:水稻(Oryza sativa)DELLA蛋白SLR1充当赤霉素(GA)信号的阻遏物。 GID1对GA的感知会导致涉及F-box蛋白GID2的SLR1蛋白降解;这会触发与GA相关的反应,例如枝条伸长和种子发芽。在GA不敏感和GA生物合成突变体中,SLENDER RICE1(SLR1)积累到高水平,而侏儒症的严重程度通常与SLR1积累的水平相关。 GA不敏感的F-box突变体gid2是一个例外,它比gid1和cps等突变体显示出更小的侏儒症,即使它积累了更高水平的SLR1。通过丧失GID1功能或使用GA生物合成抑制剂治疗,可降低gid2中SLR1蛋白的水平,并增强侏儒症。相反,GID1的过量生产或GA3的处理增加了gid2中的SLR1水平并减少了侏儒症。这些结果表明,仅通过GA和GID1即可完成SLR1抑制活性的抑制,而无需F-box(GID2)功能。在Gid2突变体中,GA调控基因(例如GA-20oxidase1,GID1和SLR1)的表达行为也提供了不含GID2的GA信号的证据。基于这些观察,我们提出了不需要DELLA蛋白降解的GA抑制释放模型。

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