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.
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.
Project description:Growth in dense stands induces shade avoidance responses. Early responses to neighbors seem to be assoctaed with touch, not light signalling. We studied gene expression in petioles during early canopy development when leaf hyponasty was visible but altered phytochrome signalling was not yet detectable.
Project description:Shade avoidance syndrome (SAS) is a strategy of major adaptive significance that includes the elongation of vegetative structures and leaf hyponasty. Major transcriptional rearrangements underlie for the reallocation of resources to elongate vegetative structures and redefine the plant architecture under shade to compete for photosynthesis light. BBX28 is a transcription factor involved in seedling de-etiolation and flowering in Arabidopsis thaliana, but its function in the SAS is completely unknown. Here we studied the function of BBX28 in the regulation of gene expression under simulated shade conditions.
Project description:Growth in dense stands induces shade avoidance responses. Early responses to neighbors seem to be assoctaed with touch, not light signalling. We studied gene expression in petioles during early canopy development when leaf hyponasty was visible but altered phytochrome signalling was not yet detectable. Plants were grown in small pots that were either kept single, or put in a high density of 2066 plants/m2. Gene expression measured in petioles when canopies had reached a leaf area index of 0.9.
Project description:Plants grown at high densities perceive a decrease in the red to far-red (R:FR) ratio of incoming light, resulting from absorption of red light by canopy leaves and reflection of far-red light from neighboring plants. These changes in light quality trigger a series of responses known collectively as the shade avoidance syndrome. During shade avoidance, stems elongate at the expense of leaf and storage organ expansion, there is reduced branching, and flowering is accelerated. We identified several loci in Arabidopsis, mutations in which lead to plants defective in multiple shade avoidance outputs. Here we describe SAV3, an aminotransferase, and show that SAV3 catalyzes the formation of indole-3-pyruvic acid (IPA) from L-tryptophan (L-Trp), the first step in a previously proposed, but uncharacterized, auxin biosynthetic pathway. This pathway can be rapidly deployed to biosynthesize auxin at the high levels required to initiate the multiple changes in body plan associated with shade avoidance. Experiment Overall Design: Wild type Col-0, sav3-2 and sav1-1 seedlings were used here. They were treated with or without 1hr of low R:FR light (R:FR ratio=0.7). Three independent biological replicates were used.
Project description:In seedlings, the induction of shade avoidance syndrome (SAS) involves a rapid up-regulation for known shade marker genes and subsequently activates an interacting network of various hormones that will eventually lead to cell elongation. We found that the B-box protein AtBBX24 have positive effects on the SAS (positive regulators). Global expression analysis of col and bbx24 seedlings reveals that a large number of genes involved in hormonal signaling pathways are positively regulated by BBX24 in response to simulated shade.
Project description:Plants grown at high densities perceive a decrease in the red to far-red (R:FR) ratio of incoming light, resulting from absorption of red light by canopy leaves and reflection of far-red light from neighboring plants. These changes in light quality trigger a series of responses known collectively as the shade avoidance syndrome. During shade avoidance, stems elongate at the expense of leaf and storage organ expansion, there is reduced branching, and flowering is accelerated. We identified several loci in Arabidopsis, mutations in which lead to plants defective in multiple shade avoidance outputs. Here we describe SAV3, an aminotransferase, and show that SAV3 catalyzes the formation of indole-3-pyruvic acid (IPA) from L-tryptophan (L-Trp), the first step in a previously proposed, but uncharacterized, auxin biosynthetic pathway. This pathway can be rapidly deployed to biosynthesize auxin at the high levels required to initiate the multiple changes in body plan associated with shade avoidance. Keywords: shade avoidance auxin brassinosteroid
Project description:Shade can trigger the shade avoidance syndrome (SAS) in shade-intolerant species, which cause exaggerated growth and affect crop yield. We report that Arabidopsis transcription factors bZIP59 negatively regulate SAS. To identify direct targets of bZIP59 at the genome-wide level, we performed ChIP-Seq using ProbZIP59::bZIP59-GFP/bzip59 transgenic plants under white light or transferred to shade conditions for 2 hours. Our results indicated shade light dramatically increased the DNA binding ability of bZIP59, and shade-enhanced binding of bZIP59 majorly located around transcriptional start site (TSS) of genes.