Abstract

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.

Highlights

  • Light is one of the most important factors for plant survival and production

  • These results suggest that ER in Col-0 ecotype makes a contribution to shade avoidance syndrome

  • The results showed that, similar to shade avoidance syndrome, hypocotyl elongation of both Col-0 and er-3 is enhanced by high temperature even in the white light condition, and hypocotyl length of er-3 is rescued similar to that of Col-0 by the same high temperature treatment, indicating that endogenous auxin level is essential for ER-modulated hypocotyl elongation

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Summary

Introduction

Plants always grow closely to one another Under these conditions, red light wavelengths is been absorbed while the far red light wavelengths is reflected by the leaves of the neighboring plants, resulting in reduction of red:far red (R:FR) light ratio and light intensity, referred to as shade condition. Plants must accelerate their growth in order to maintain their height at least as tall as their neighboring plants to succeed in light sensing competition conditions (Ballaré, 1999). In this process, plants have to expend more energy to support their elongation growth at the expense of leaf development, seed number and yield reduction. Arabidopsis and most crops show typical phenotypes of SAR, while some other plants display shade tolerance phenotype mimicking the phenotypes of the plants in the white light condition (Valladares and Niinemets, 2008; Carriedo et al, 2016)

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