Auxin and Gibberellins Are Required for the Receptor-Like Kinase ERECTA Regulated Hypocotyl Elongation in Shade Avoidance in Arabidopsis.
Auxin and Gibberellins Are Required for the Receptor-Like Kinase ERECTA Regulated Hypocotyl Elongation in Shade Avoidance in Arabidopsis.
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拟南芥避荫过程中受体样激酶 ERECTA 调节下胚轴伸长需要生长素和赤霉素
DOI：
10.3389/fpls.2018.00124
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发表时间：
2018
影响因子：
5.6
通讯作者：
Yang W
中科院分区：
文献类型：
--
作者：
Du J;Jiang H;Sun X;Li Y;Liu Y;Sun M;Fan Z;Cao Q;Feng L;Shang J;Shu K;Liu J;Yang F;Liu W;Yong T;Wang X;Yuan S;Yu L;Liu C;Yang W
植物在自然条件下生长时使用避阴策略来逃避树冠的阴影。先前的研究表明，拟南芥受体样激酶ERECTA（ER）与避荫综合征有关。然而，ER通过促进下胚轴伸长调节SAR的机制尚不清楚。在这里，我们报告说，ER调节下胚轴伸长避荫需要生长素和赤霉素（GAs）。T-DNA插入ER突变体er-3的下胚轴长度比Col-0野生型短。启动子：：GUS染色分析表明，ER及其同源基因ERECTA-LIKE 1（ERL 1）和ERECTA-LIKE 2（ERL 2）在幼苗中差异表达，其中只有ER在遮荫处理下胚轴中表达上调最明显。采用垂直培养的拟南芥幼苗进行的外源取食实验表明，吲哚乙酸（IAA）对er-3下胚轴的生长有一定的促进作用，但与Col-0相比，er-3对不同浓度的IAA相对不敏感。白色光条件下，高温对er-3下胚轴伸长的促进作用与Col-0相似，但生长素转运抑制剂1-N-naphthylphthalamic acid（NPA）对下胚轴伸长的影响不显著。在遮荫条件下，外源GA 3促进了er-3和野生型下胚轴的伸长，GA 3生物合成抑制剂PAC严重抑制了Col-0和er-3下胚轴的伸长。进一步分析表明，生长素生物合成抑制剂尤卡坦和L-犬尿氨酸显著抑制er-3的下胚轴伸长，而尤卡坦对er-3的抑制作用比Col-0更强。调节生长素稳态和信号传导以及GA稳态的基因的相对表达在er-3中比在Col-0中少。此外，遗传学证据表明ER调控下胚轴的伸长依赖于光敏色素B（PHYB）。总体而言，我们建议ER调节避荫促进下胚轴伸长是PHYB依赖的，需要生长素和GAs。
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 ER mutant er-3 shows a less hypocotyl length than that in Col-0 wild type. Promoter::GUS staining analysis shows that ER and its paralogous genes ERECTA-LIKE1 (ERL1) and ERECTA-LIKE2 (ERL2) are differentially expressed in the seedlings, of which only ER 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 er-3 is partially promoted by indol-3-acetic acid (IAA), while it is relatively insensitive of er-3 to various concentrations of IAA than that of Col-0. Hypocotyl elongation of er-3 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-N-naphthylphthalamic acid (NPA). Exogenous GA3 increased the hypocotyl elongation of both er-3 and the wild type in the shade condition, and the GA3 biosynthesis inhibitor paclobutrazol (PAC) severely inhibits the hypocotyl elongation of Col-0 and er-3. Further analysis showed that auxin biosynthesis inhibitors yucasin and L-kynurenine remarkably inhibited the hypocotyl elongation of er-3 while yucasin shows a more severe inhibition to er-3 than Col-0. Relative expression of genes regulating auxin homeostasis and signaling, and GA homeostasis is less in er-3 than that in Col-0. Furthermore, genetic evidences show that ER 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.
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