Dataset Information

The receptor-like kinase ERECTA contributes to the shade-avoidance syndrome in a background-dependent manner.

ABSTRACT:

Background and aims

Plants growing at high densities perceive a decrease in the red to far-red (R/FR) ratio of incoming light. These changes in light quality trigger a suite of responses collectively known as the shade-avoidance syndrome (SAS) including hypocotyl and stem elongation, inhibition of branching and acceleration of flowering.

Methods

Quantitative trait loci (QTLs) were mapped for hypocotyl length to end-of-day far-red (EOD), a simulated shade-avoidance response, in recombinant inbred line (RIL) populations of Arabidopsis thaliana seedlings, derived from Landsberg erecta (Ler) and three accessions (Columbia, Col; Nossen, No-0; and Cape Verde Islands, Cvi-0).

Key results

Five loci were identified as being responsible for the EOD response, with a positive contribution of Ler alleles on the phenotype independently of the RIL population. Quantitative complementation analysis and transgenic lines showed that PHYB is the candidate gene for EODRATIO5 in the Ler × Cvi-0 RIL population, but not for two co-localized QTLs, EODRATIO1 and EODRATIO2 mapped in the Ler × No-0 and Ler × Col RIL populations, respectively. The ERECTA gene was also implicated in the SAS in a background-dependent manner. For hypocotyl length EOD response, a positive contribution of erecta alleles was found in Col and Van-0, but not in Ler, Cvi-0, Hir-1 or Ws. Furthermore, pleiotropic effects of ERECTA in the EOD response were also detected for petiole and lamina elongation, hyponastic growth, and flowering time.

Conclusions

The results show that the analysis of multiple mapping populations leads to a better understanding of the SAS genetic architecture. Moreover, the background- and trait-dependent contribution of ERECTA in the SAS suggest that its function in shaded natural environments may be relevant for some populations in different phases of plant development. It is proposed that ERECTA is involved in canalization processes buffering the genetic variation of the SAS against environmental light fluctuations.

SUBMITTER: Kasulin L

PROVIDER: S-EPMC3631326 | biostudies-literature | 2013 May

REPOSITORIES: biostudies-literature

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Publications

The receptor-like kinase ERECTA contributes to the shade-avoidance syndrome in a background-dependent manner.

Kasulin Luciana L Agrofoglio Yamila Y Botto Javier F JF

Annals of botany 20130226 5

<h4>Background and aims</h4>Plants growing at high densities perceive a decrease in the red to far-red (R/FR) ratio of incoming light. These changes in light quality trigger a suite of responses collectively known as the shade-avoidance syndrome (SAS) including hypocotyl and stem elongation, inhibition of branching and acceleration of flowering.<h4>Methods</h4>Quantitative trait loci (QTLs) were mapped for hypocotyl length to end-of-day far-red (EOD), a simulated shade-avoidance response, in rec ...[more]

PMID: 23444123

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Project description: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.

Project description:Plants grown under a canopy recognize changes in light quality and modify their growth patterns; this modification is known as shade avoidance syndrome. In leaves, leaf blade expansion is suppressed, whereas petiole elongation is promoted under the shade. However, the mechanisms that control these responses are largely unclear. Here, we demonstrated that both auxin and brassinosteroid (BR) are required for the normal leaf responses to shade. The microarray analysis of leaf blades and petioles treated with end-of-day far-red light (EODFR) revealed that almost half of the genes induced by the treatment in both parts were previously identified as auxin-responsive genes. Likewise, BR-responsive genes were overrepresented in the EODFR-induced genes. Hence, the auxin and BR responses were elevated by EODFR treatment in both leaf blades and petioles, although opposing growth responses were observed in these two parts. The analysis of the auxin-deficient doc1/big mutant and BR-deficient rot3/cyp90c1 mutant further indicates that auxin and BR were equally required for the normal petiole elongation response to the shade stimulus. In addition, the spotlight irradiation experiment revealed that phytochrome in leaf blades but not that in petioles regulated petiole elongation, which was probably mediated through regulation of the auxin/BR responses in petioles. On the basis of these findings, we conclude that auxin and BR cooperatively promote petiole elongation in response to the shade stimulus under the control of phytochrome in the leaf blade. The WT seedlings were grown for 19 days under continuous white light condition before experimental treatment with three light conditions. Seedlings were either maintained in white light for 2 h (WL), incubated in the dark condition for 2 h (D), or experienced a pulse irradiation of FR light before incubated in the dark condition for 2 h (FRD). Total RNAs were separately prepared from leaf blades and petioles after each light treatment. Three independent biological replicates were used.

Dataset Information

The receptor-like kinase ERECTA contributes to the shade-avoidance syndrome in a background-dependent manner.

Background and aims

Methods

Key results

Conclusions

Publications

The receptor-like kinase ERECTA contributes to the shade-avoidance syndrome in a background-dependent manner.

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