Hormonal Regulation in Shade Avoidance

At high vegetation density, shade-intolerant plants sense a reduction in the red (660 nm) to far-red (730 nm) light ratio (R/FR) in addition to a general reduction in light intensity. These light signals trigger a spectrum of morphological changes manifested by growth of stem-like tissue (hypocotyl, petiole, etc.) instead of harvestable organs (leaves, fruits, seeds, etc.)—namely, shade avoidance syndrome (SAS). Common phenotypical changes related to SAS are changes in leaf hyponasty, an increase in hypocotyl and internode elongation and extended petioles. Prolonged shade exposure leads to early flowering, less branching, increased susceptibility to insect herbivory, and decreased seed yield. Thus, shade avoidance significantly impacts on agronomic traits. Many genetic and molecular studies have revealed that phytochromes, cryptochromes and UVR8 (UV-B photoreceptor protein) monitor the changes in light intensity under shade and regulate the stability or activity of phytochrome-interacting factors (PIFs). PIF-governed modulation of the expression of auxin biosynthesis, transporter and signaling genes is the major driver for shade-induced hypocotyl elongation. Besides auxin, gibberellins, brassinosteroids, and ethylene are also required for shade-induced hypocotyl or petiole elongation growth. In leaves, accumulated auxin stimulates cytokinin oxidase expression to break down cytokinins and inhibit leaf growth. In the young buds, shade light promotes the accumulation of abscisic acid to repress branching. Shade light also represses jasmonate- and salicylic acid-induced defense responses to balance resource allocation between growth and defense. Here we will summarize recent findings relating to such hormonal regulation in SAS in Arabidopsis thaliana, Brassica rapa, and certain crops.