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E3 小泛素样修饰蛋白连接酶AtSIZ1在拟南芥种子萌发过程中发挥作用。

The E3 SUMO ligase AtSIZ1 functions in seed germination in Arabidopsis.

作者信息

Kim Sung-Il, Kwak Jun Soo, Song Jong Tae, Seo Hak Soo

机构信息

Department of Plant Science, Research Institute for Agriculture and Life Sciences, and Plant Genomics and Breeding Institute, Seoul National University, Seoul, 151-921, Korea.

School of Applied Biosciences, Kyungpook National University, Daegu, 702-701, Korea.

出版信息

Physiol Plant. 2016 Nov;158(3):256-271. doi: 10.1111/ppl.12462. Epub 2016 Jun 6.

Abstract

Seed germination is an important stage in the lifecycle of a plant because it determines subsequent vegetative growth and reproduction. Here, we show that the E3 SUMO ligase AtSIZ1 regulates seed dormancy and germination. The germination rates of the siz1 mutants were less than 50%, even after a short period of ripening. However, their germination rates increased to wild-type levels after cold stratification or long periods of ripening. In addition, exogenous gibberellin (GA) application improved the germination rates of the siz1 mutants to the wild-type level. In transgenic plants, suppression of AtSIZ1 caused rapid post-translational decay of SLEEPY1 (SLY1), a positive regulator of GA signaling, during germination, and inducible AtSIZ1 overexpression led to increased SLY1 levels. In addition, overexpressing wild-type SLY1 in transgenic sly1 mutants increased their germination ratios to wild-type levels, whereas the germination ratio of transgenic sly1 mutants overexpressing mSLY1 was similar to that of sly1. The germination ratios of siz1 mutant seeds in immature developing siliques were much lower than those of the wild-type. Moreover, SLY1 and DELAY OF GERMINATION 1 (DOG1) transcript levels were reduced in the siz1 mutants, whereas the transcript levels of DELLA and ABSCISIC ACID INSENSITIVE 3 (ABI3) were higher than those of the wild-type. Taken together, these results indicate that the reduced germination of the siz1 mutants results from impaired GA signaling due to low SLY1 levels and activity, as well as hyperdormancy due to high levels of expression of dormancy-related genes including DOG1.

摘要

种子萌发是植物生命周期中的一个重要阶段,因为它决定了后续的营养生长和繁殖。在这里,我们表明E3 SUMO连接酶AtSIZ1调节种子休眠和萌发。即使经过短时间的成熟,siz1突变体的萌发率仍低于50%。然而,经过冷层积处理或长时间成熟后,它们的萌发率提高到了野生型水平。此外,外源施加赤霉素(GA)可将siz1突变体的萌发率提高到野生型水平。在转基因植物中,AtSIZ1的抑制导致萌发过程中GA信号的正向调节因子SLEEPY1(SLY1)的快速翻译后降解,而诱导型AtSIZ1过表达导致SLY1水平升高。此外,在转基因sly1突变体中过表达野生型SLY1可将其萌发率提高到野生型水平,而过表达mSLY1的转基因sly1突变体的萌发率与sly1相似。未成熟发育的角果中siz1突变体种子的萌发率远低于野生型。此外,siz1突变体中SLY1和萌发延迟1(DOG1)的转录水平降低,而DELLA和脱落酸不敏感3(ABI3)的转录水平高于野生型。综上所述,这些结果表明,siz1突变体萌发率降低是由于SLY1水平和活性低导致GA信号受损,以及包括DOG1在内的休眠相关基因高表达导致的过度休眠。

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