Melatonin is a pleiotropic molecule with multiple functions in plants. Since the discovery of melatonin in plants, numerous studies have provided insight into the biosynthesis, catabolism, and physiological and biochemical functions of this important molecule. Here, we describe the biosynthesis of melatonin from tryptophan, as well as its various degradation pathways in plants. The identification of a putative melatonin receptor in plants has led to the hypothesis that melatonin is a hormone involved in regulating plant growth, aerial organ development, root morphology, and the floral transition. The universal antioxidant activity of melatonin and its role in preserving chlorophyll might explain its anti‐senescence capacity in aging leaves. An impressive amount of research has focused on the role of melatonin in modulating postharvest fruit ripening by regulating the expression of ethylene‐related genes. Recent evidence also indicated that melatonin functions in the plant's response to biotic stress, cooperating with other phytohormones and well‐known molecules such as reactive oxygen species and nitric oxide. Finally, great progress has been made towards understanding how melatonin alleviates the effects of various abiotic stresses, including salt, drought, extreme temperature, and heavy metal stress. Given its diverse roles, we propose that melatonin is a master regulator in plants.

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The formation of Casparian strips and suberin lamellae at the endodermis limits the free diffusion of nutrients and harmful substances via the apoplastic space between the soil solution and the stele in roots [1-3]. Casparian strips are ring-like lignin polymers deposited in the middle of anticlinal cell walls between endodermal cells and fill the gap between them [4-6]. Suberin lamellae are glycerolipid polymers covering the endodermal cells and likely function as a barrier to limit transmembrane movement of apoplastic solutes into the endodermal cells [7, 8]. However, the current knowledge on the formation of these two distinct endodermal barriers and their regulatory role in nutrient transport is still limited. Here, we identify an uncharacterized gene, LOTR1, essential for Casparian strip formation in Arabidopsis thaliana. The lotr1 mutants display altered localization of CASP1, an essential protein for Casparian strip formation [9], disrupted Casparian strips, ectopic suberization of endodermal cells, and low accumulation of shoot calcium (Ca). Degradation by expression of a suberin-degrading enzyme in the mutants revealed that the ectopic suberization at the endodermal cells limits Ca transport through the transmembrane pathway, thereby causing reduced Ca delivery to the shoot. Moreover, analysis of the mutants showed that suberin lamellae function as an apoplastic diffusion barrier to the stele at sites of lateral root emergence where Casparian strips are disrupted. Our findings suggest that the transmembrane pathway through unsuberized endodermal cells, rather than the sites of lateral root emergence, mediates the transport of apoplastic substances such as Ca into the xylem.

Ammonium (NH(4)(+)) is a ubiquitous intermediate of nitrogen metabolism but is notorious for its toxic effects on most organisms. Extensive studies of the underlying mechanisms of NH(4)(+) toxicity have been reported in plants, but it is poorly understood how plants acclimate to high levels of NH(4)(+). Here, we identified an Arabidopsis (Arabidopsis thaliana) mutant, ammonium overly sensitive1 (amos1), that displays severe chlorosis under NH(4)(+) stress. Map-based cloning shows amos1 to carry a mutation in EGY1 (for ethylene-dependent, gravitropism-deficient, and yellow-green-like protein1), which encodes a plastid metalloprotease. Transcriptomic analysis reveals that among the genes activated in response to NH(4)(+), 90% are regulated dependent on AMOS1/EGY1. Furthermore, 63% of AMOS1/EGY1-dependent NH(4)(+)-activated genes contain an ACGTG motif in their promoter region, a core motif of abscisic acid (ABA)-responsive elements. Consistent with this, our physiological, pharmacological, transcriptomic, and genetic data show that ABA signaling is a critical, but not the sole, downstream component of the AMOS1/EGY1-dependent pathway that regulates the expression of NH(4)(+)-responsive genes and maintains chloroplast functionality under NH(4)(+) stress. Importantly, abi4 mutants defective in ABA-dependent and retrograde signaling, but not ABA-deficient mutants, mimic leaf NH(4)(+) hypersensitivity of amos1. In summary, our findings suggest that an NH(4)(+)-responsive plastid retrograde pathway, which depends on AMOS1/EGY1 function and integrates with ABA signaling, is required for the regulation of expression of NH(4)(+)-responsive genes that maintain chloroplast integrity in the presence of high NH(4)(+) levels.