突变体
生物
减压
侏儒症
赤霉素
抑制因子
细胞生物学
基因
心理压抑
生物化学
遗传学
基因表达
作者
Miyako Ueguchi‐Tanaka,Ko Hirano,Yasuko Hasegawa,Hidemi Kitano,Makoto Matsuoka
出处
期刊:The Plant Cell
[Oxford University Press]
日期:2008-09-01
卷期号:20 (9): 2437-2446
被引量:113
标识
DOI:10.1105/tpc.108.061648
摘要
Abstract 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.
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