USDA-ARS, Wheat Genetics; Quality Physiology and Disease Research Unit, Washington State University, Pullman, WA, USA.
Plant Signal Behav. 2011 Jun;6(6):831-3. doi: 10.4161/psb.6.6.15164. Epub 2011 Jun 1.
We previously reported that the SLEEPY1 (SLY1) homolog, F-box gene SNEEZY/SLEEPY2 (SNE/SLY2), can partly replace SLY1 in gibberellin (GA) hormone signaling through interaction with DELLAs RGA and GAI. To determine whether SNE normally functions in GA signaling, we characterized the phenotypes of two T-DNA alleles, sne-t2 and sne-t3. These mutations result in no apparent vegetative phenotypes, but do result in increased ABA sensitivity in seed germination. Double mutants sly1-t2 sne-t2 and sly1-t2 sne-t3 result in a significant decrease in plant fertility and final plant height compared to sly1-t2. The fact that sne mutations have an additive effect with sly1 suggests that SNE normally functions as a redundant positive regulator of GA signaling.
我们之前报道过,SLEEPY1(SLY1)同源物 F-box 基因 SNEEZY/SLEEPY2(SNE/SLY2)可以通过与 DELLAs RGA 和 GAI 的相互作用部分替代 SLY1 在赤霉素(GA)激素信号转导中发挥作用。为了确定 SNE 是否在 GA 信号转导中正常发挥作用,我们对两个 T-DNA 等位基因 sne-t2 和 sne-t3 的表型进行了表征。这些突变导致没有明显的营养表型,但导致种子萌发中 ABA 敏感性增加。与 sly1-t2 相比,sly1-t2 sne-t2 和 sly1-t2 sne-t3 的双突变体导致植物育性和最终株高显著降低。sne 突变与 sly1 具有累加效应的事实表明,SNE 通常作为 GA 信号转导的冗余正调节剂发挥作用。