Stanga John P, Morffy Nicholas, Nelson David C
Department of Genetics, University of Georgia, Athens, GA, 30602, USA.
Planta. 2016 Jun;243(6):1397-406. doi: 10.1007/s00425-015-2458-2. Epub 2016 Jan 11.
SMAX1 and SMXL2 control seedling growth, demonstrating functional redundancy within a gene family that mediates karrikin and strigolactone responses. Strigolactones (SLs) are plant hormones with butenolide moieties that control diverse aspects of plant growth, including shoot branching. Karrikins (KARs) are butenolide molecules found in smoke that enhance seed germination and seedling photomorphogenesis. In Arabidopsis thaliana, SLs and KARs signal through the α/β hydrolases D14 and KAI2, respectively. The F-box protein MAX2 is essential for both signaling pathways. SUPPRESSOR OF MAX2 1 (SMAX1) plays a prominent role in KAR-regulated growth downstream of MAX2, and SMAX1-LIKE genes SMXL6, SMXL7, and SMXL8 mediate SL responses. We previously found that smax1 loss-of-function mutants display constitutive KAR response phenotypes, including reduced seed dormancy and hypersensitive growth responses to light in seedlings. However, smax1 seedlings remain slightly responsive to KARs, suggesting that there is functional redundancy in karrikin signaling. SMXL2 is a strong candidate for this redundancy because it is the closest paralog of SMAX1, and because its expression is regulated by KAR signaling. Here, we present evidence that SMXL2 controls hypocotyl growth and expression of the KAR/SL transcriptional markers KUF1, IAA1, and DLK2 redundantly with SMAX1. Hypocotyl growth in the smax1 smxl2 double mutant is insensitive to KAR and SL, and etiolated smax1 smxl2 seedlings have reduced hypocotyl elongation. However, smxl2 has little or no effect on seed germination, leaf shape, or petiole orientation, which appear to be predominantly controlled by SMAX1. Neither SMAX1 nor SMXL2 affect axillary branching or inflorescence height, traits that are under SL control. These data support the model that karrikin and strigolactone responses are mediated by distinct subclades of the SMXL family, and further the case for parallel butenolide signaling pathways that evolved through ancient KAI2 and SMXL duplications.
SMAX1和SMXL2控制幼苗生长，证明了在介导卡里金和独脚金内酯反应的基因家族中存在功能冗余。独脚金内酯（SLs）是具有丁烯内酯部分的植物激素，可控制植物生长的多个方面，包括枝条分枝。卡里金（KARs）是在烟雾中发现的丁烯内酯分子，可促进种子萌发和幼苗光形态建成。在拟南芥中，SLs和KARs分别通过α/β水解酶D14和KAI2进行信号传导。F-box蛋白MAX2对这两种信号通路都至关重要。MAX2的抑制因子1（SMAX1）在MAX2下游的KAR调节生长中起重要作用，而类SMAX1基因SMXL6、SMXL7和SMXL8介导SL反应。我们之前发现，smax1功能缺失突变体表现出组成型KAR反应表型，包括种子休眠减少和幼苗对光的超敏生长反应。然而，smax1幼苗对KARs仍有轻微反应，这表明卡里金信号传导中存在功能冗余。SMXL2是这种冗余的有力候选者，因为它是SMAX1最接近的旁系同源物，并且其表达受KAR信号传导调节。在这里，我们提供证据表明，SMXL2与SMAX1一起冗余控制下胚轴生长以及KAR/SL转录标记KUF1、IAA1和DLK2的表达。smax1 smxl2双突变体的下胚轴生长对KAR和SL不敏感，黄化的smax1 smxl2幼苗的下胚轴伸长减少。然而，smxl2对种子萌发、叶片形状或叶柄方向几乎没有影响，这些似乎主要由SMAX1控制。SMAX1和SMXL2都不影响腋芽分枝或花序高度，这些性状受SL控制。这些数据支持了卡里金和独脚金内酯反应由SMXL家族不同亚分支介导的模型，并进一步证明了通过古老的KAI2和SMXL复制进化而来的平行丁烯内酯信号通路的情况。
