Figure 1.6:

Figure 1.5:

)

Neighbor proximity signals, including reflected FR and horizontal blue light gradients trigger early responses including elongation and bending toward canopy gaps, acting via phyB and phots, respectively. Shading results in progressive inactivation of phyB, crys, and UVR8, leading to enhanced activity of (i) growth-promoting PIF transcription factors [12], and (ii) the E3 ligase complex COP1/SPA, which controls the ubiquitination and subsequent degradation of the growth-inhibiting transcription factor HY5 [93]. PIFs trigger elongation responses through the canonical PIF–auxin (IAA) pathway (red arrow). An intricate network of interactions downstream of the photoreceptors allows plants to incorporate information from multiple light signals to optimize their response. For example, cry inactivation under low blue light potentiates the elongation response triggered by low R:FR via (i) increased PIF abundance and activity, and (ii) attenuation of the low R:FR-induced negative-feedback loop that depends on negative regulators of PIF activity. The latter effect of cry1 inactivation is mediated by reduced gene expression of negative regulators and reduced HFR1 levels through a COP1-dependent mechanism [17]. In addition, low R:FR [20] and low blue [33] increase the intensity of phototropic responses (mediated by phots) when the plant is shaded by other plants. This is because inactivation of phyB and cry increase PIF activity, resulting in enhanced auxin signaling in the hypocotyl and, upon phototropic stimulation, a steeper auxin signaling gradient across the organ. In canopy gaps, solar UV radiation, acting via UVR8, attenuates elongation responses to low R:FR ratios by promoting the degradation of PIF4 and PIF5 and by stabilizing growth-repressing DELLA proteins [25]. Photoactivated UVR8 interacts with COP1, which reduces the activity of PIFs via at least two mechanisms: (i) by preventing a (noncanonical) effect of COP1 that increases the stability of PIF5 [31], and (ii) by stabilizing the negative regulator HFR1 (a COP1 substrate) [32]. In addition to altering auxin metabolism and transport, PIFs and COP1/SPA activate a suite of changes in GA (details in Fernández-Milmanda and Ballaré 2021, fig. 3) and JA signaling (details in Fernández-Milmanda and Ballaré 2021, fig. 4), which leads to a major reconfiguration of the growth and defense phenotype. Symbols: indicates negative regulation; → indicates positive regulation. Abbreviations: COP1, CONSTITUTIVELY PHOTOMORPHOGENIC 1; cry, cryptochrome; FAR1, FAR-RED-IMPAIRED RESPONSE 1; FHY3, FAR-RED ELONGATED HYPOCOTYL 3; FR, far-red; GA, gibberellins; HFR1, LONG HYPOCOTYL IN FAR-RED 1; HY5, ELONGATED HYPOCOTYL 5; IAA, indole-3-acetic acid; JA, jasmonic acid; JAZ, JASMONATE ZIM-DOMAIN; PAR1, PHYTOCHROME RAPIDLY REGULATED 1; phot, phototropin; phyB, phytochrome B; PIF, PHYTOCHROME INTERACTING FACTOR; R, red; SPA, SUPPRESSOR OF PHYA-105; UVR8, UV RESISTANCE LOCUS 8.

Introduction