Du Junbo, Jiang Hengke, Sun Xin, Li Yan, Liu Yi, Sun Mengyuan, Fan Zhou, Cao Qiulin, Feng Lingyang, Shang Jing, Shu Kai, Liu Jiang, Yang Feng, Liu Weiguo, Yong Taiwen, Wang Xiaochun, Yuan Shu, Yu Liang, Liu Chunyan, Yang Wenyu
College of Agronomy, Sichuan Agricultural University, Chengdu, China.
Sichuan Engineering Research Center for Crop Strip Intercropping System, Sichuan Agricultural University, Chengdu, China.
Front Plant Sci. 2018 Feb 7;9:124. doi: 10.3389/fpls.2018.00124. eCollection 2018.
Plants use shade avoidance strategy to escape the canopy shade when grown under natural conditions. Previous studies showed that the Arabidopsis receptor-like kinase ERECTA (ER) is involved in shade avoidance syndrome. However, the mechanisms of ER in modulating SAR by promoting hypocotyl elongation are unknown yet. Here, we report that ER regulated hypocotyl elongation in shade avoidance requires auxin and gibberellins (GAs). The T-DNA insertional mutant shows a less hypocotyl length than that in Col-0 wild type. Promoter::GUS staining analysis shows that and its paralogous genes () and () are differentially expressed in the seedlings, of which only is most obviously upregulated in the hypocotyl by shade treatment. Exogenous feeding assay by using media-application with vertical-grown of Arabidopsis seedlings showed that the hypocotyl length of is partially promoted by indol-3-acetic acid (IAA), while it is relatively insensitive of to various concentrations of IAA than that of Col-0. Hypocotyl elongation of is promoted similar to that of Col-0 by high temperature in the white light condition, but the elongation was not significantly affected by the treatment of the auxin transport inhibitor 1--naphthylphthalamic acid (NPA). Exogenous GA3 increased the hypocotyl elongation of both and the wild type in the shade condition, and the GA3 biosynthesis inhibitor paclobutrazol (PAC) severely inhibits the hypocotyl elongation of Col-0 and . Further analysis showed that auxin biosynthesis inhibitors yucasin and L-kynurenine remarkably inhibited the hypocotyl elongation of while yucasin shows a more severe inhibition to than Col-0. Relative expression of genes regulating auxin homeostasis and signaling, and GA homeostasis is less in than that in Col-0. Furthermore, genetic evidences show that regulated hypocotyl elongation is dependent of PHYTOCHROME B (PHYB). Overall, we propose that ER regulated shade avoidance by promoting hypocotyl elongation is PHYB-dependent and requires auxin and GAs.
植物在自然条件下生长时会采用避荫策略以逃离树冠遮荫。先前的研究表明，拟南芥类受体激酶ERECTA（ER）参与避荫综合征。然而，ER通过促进下胚轴伸长来调节避荫反应（SAR）的机制尚不清楚。在此，我们报道ER在避荫反应中调节下胚轴伸长需要生长素和赤霉素（GA）。T-DNA插入突变体的下胚轴长度比Col-0野生型短。启动子::GUS染色分析表明，其同源基因ERL1和ERL2在幼苗中差异表达，其中只有ERL1在遮荫处理的下胚轴中上调最为明显。通过在垂直生长的拟南芥幼苗培养基中添加外源物质进行测定，结果表明，吲哚-3-乙酸（IAA）部分促进了ERL1的下胚轴长度，而与Col-0相比，ERL1对不同浓度的IAA相对不敏感。在白光条件下，高温促进ERL1的下胚轴伸长与Col-0相似，但生长素运输抑制剂1-萘基邻苯二甲酸（NPA）处理对其伸长没有显著影响。外源GA3增加了遮荫条件下ERL1和野生型的下胚轴伸长，而GA3生物合成抑制剂多效唑（PAC）严重抑制了Col-0和ERL1的下胚轴伸长。进一步分析表明，生长素生物合成抑制剂玉蜀黍素和L-犬尿氨酸显著抑制ERL1的下胚轴伸长，而玉蜀黍素对ERL1的抑制作用比对Col-0更严重。ERL1中调节生长素稳态和信号传导以及GA稳态的基因相对表达量低于Col-0。此外，遗传学证据表明，ERL1调节的下胚轴伸长依赖于光敏色素B（PHYB）。总体而言，我们提出ER通过促进下胚轴伸长来调节避荫反应是依赖于PHYB的，并且需要生长素和GA。
