Phototropin (phot) receptor kinases play important roles in promoting plant growth by controlling light-capturing processes, such as phototropism. Phototropism is mediated through the action of NON-PHOTOTROPIC HYPOCOTYL3 (NPH3), which is dephosphorylated following phot activation. However, the functional significance of this early signaling event remains unclear. Here, we show that the onset of phototropism in dark-grown (etiolated) seedlings of Arabidopsis (Arabidopsis thaliana) and tomato (Solanum lycopersicum) is enhanced by greening (deetiolation). Red and blue light were equally effective in promoting phototropism in Arabidopsis, consistent with our observations that deetiolation by phytochrome or cryptochrome was sufficient to enhance phototropism. Increased responsiveness did not result from an enhanced sensitivity to the phytohormone auxin, nor does it involve the phot-interacting protein, ROOT PHOTOTROPISM2. Instead, deetiolated seedlings showed attenuated levels of NPH3 dephosphorylation and diminished relocalization of NPH3 from the plasma membrane during phototropism. Likewise, etiolated seedlings that lack the PHYTOCHROME-INTERACTING FACTORS (PIFs) PIF1, PIF3, PIF4, and PIF5 displayed reduced NPH3 dephosphorylation and enhanced phototropism, consistent with their constitutive photomorphogenic phenotype in darkness. Phototropic enhancement could also be achieved in etiolated seedlings by lowering the light intensity to diminish NPH3 dephosphorylation. Thus, phototropism is enhanced following deetiolation through the modulation of a phosphorylation rheostat, which in turn sustains the activity of NPH3. We propose that this dynamic mode of regulation enables young seedlings to maximize their establishment under changing light conditions, depending on their photoautotrophic capacity.

Rising temperatures during growing seasons coupled with altered precipitation rates presents a challenging task of improving crop productivity for overcoming such altered weather patterns and cater to a growing population. Light is a critical environmental factor that exerts a powerful influence on plant growth and development ranging from seed germination to flowering and fruiting. Higher plants utilize a suite of complex photoreceptor proteins to perceive surrounding red/far-red (phytochromes), blue/UV-A (cryptochromes, phototropins, ZTL/FKF1/LKP2), and UV-B light (UVR8). While genomic studies have also shown that light induces extensive reprogramming of gene expression patterns in plants, molecular genetic studies have shown that manipulation of one or more photoreceptors can result in modification of agronomically beneficial traits. Such information can assist researchers to engineer photoreceptors via genome editing technologies to alter expression or even sensitivity thresholds of native photoreceptors for targeting aspects of plant growth that can confer superior agronomic value to the engineered crops. Here we summarize the agronomically important plant growth processes influenced by photoreceptors in crop species, alongwith the functional interactions between different photoreceptors and phytohormones in regulating these responses. We also discuss the potential utility of synthetic biology approaches in photobiology for improving agronomically beneficial traits of crop plants by engineering designer photoreceptors.

Nitric oxide (NO) is involved in diverse plant growth processes; however, little is known about pathways regulating NO levels in plants. In this study, we isolated a NO-overproducing mutant of tomato (Solanum lycopersicum) in which hyper-accumulation of NO, associated with increase in nitric oxide synthase (NOS)-like activity, caused diminished vegetative growth of plants and showed delayed flowering. The hyper-accumulation of NO caused drastic shortening of primary root (shr) in the seedlings, while the scavenging of NO restored root elongation in shr mutant. Inhibition of NOS-like activity reduced NO levels and stimulated root elongation in the shr mutant seedlings, while inhibition of nitrate reductase (NR) activity could not rescue shr phenotype. The stimulation of NO levels in shr mutant also conferred increased resistance to pathogen Pseudomonas syringae. Application of pharmacological inhibitors regulating ubiquitin-proteasome pathway reduced NO levels and NOS-like activity and stimulated shr root elongation. Our data indicate that a signaling pathway involving regulated protein degradation likely regulates NO synthesis in tomato.

In higher plants, blue light (BL) phototropism is primarily controlled by the phototropins, which are also involved in stomatal movement and chloroplast relocation. These photoresponses are mediated by two phototropins, phot1 and phot2. Phot1 mediates responses with higher sensitivity than phot2, and phot2 specifically mediates chloroplast avoidance and dark positioning responses. Here, we report the isolation and characterization of a Nonphototropic seedling1 (Nps1) mutant of tomato (Solanum lycopersicum). The mutant is impaired in low-fluence BL responses, including chloroplast accumulation and stomatal opening. Genetic analyses show that the mutant locus is dominant negative in nature. In dark-grown seedlings of the Nps1 mutant, phot1 protein accumulates at a highly reduced level relative to the wild type and lacks BL-induced autophosphorylation. The mutant harbors a single glycine-1484-toalanine transition in the Hinge1 region of a phot1 homolog, resulting in an arginine-to-histidine substitution (R495H) in a highly conserved A9a helix proximal to the light-oxygen and voltage2 domain of the translated gene product. Significantly, the R495H substitution occurring in the Hinge1 region of PHOT1 abolishes its regulatory activity in Nps1 seedlings, thereby highlighting the functional significance of the A9a helix region in phototropic signaling of tomato.

The bilateral symmetry of a dicotyledon embryo is tightly associated with the directional flow of auxin. Disruption of polar auxin flow results in various developmental abnormalities. The pct1-2 mutant of tomato, showing polycotyledony, also has enhanced polar auxin transport in hypocotyls. Immunocytochemical analysis revealed increased PIN1 protein in pct1-2 roots and hypocotyls. The mutant also displayed an increase in PIN1 transcript levels in these organs. Our results indicate that over-accumulation of PIN1 protein is likely related to increased polar transport of auxin in the pct1-2 mutant.