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The apical hook is a developmentally regulated structure that appears in dicotyledonous seedlings when seeds germinate buried in the soil. It protects the shoot apical meristem and cotyledons from damage while the seedling is pushing upwards seeking for light, and it is formed by differential cell expansion between both sides of the upper part of the hypocotyl. Its apparent simplicity and the fact that it is dispensable when seedlings are grown in vitro have converted the apical hook in one of the favorite experimental models to study the regulation of differential growth. The involvement of hormones -especially auxin-in this process was manifested already in the early studies. Remarkably, a gradient of this hormone across the hook curvature is instrumental to complete its development, similar to what has been proposed for other processes involving the bending of an organ, such as tropic responses. In agreement with this, other hormones-mainly gibberellins and ethylene-and the light, regulate in a timely and interconnected manner the auxin gradient to promote hook development and its opening, respectively. Here, we review the latest findings obtained mainly with the apical hook of Arabidopsis thaliana, paying special attention to the molecular mechanisms for the cross-regulation between the different hormone signaling pathways that underlie this developmental process.

Due to their sessile nature, plants constantly adapt to their environment by modulating various internal plant hormone signals and distributions, as plants perceive environmental changes. Plant hormones include abscisic acid (ABA), auxins, brassinosteroids, cytokinins, ethylene, gibberellins, jasmonates, salicylic acid, and strigolactones, which collectively regulate plant growth, development, metabolism, and defense. Moreover, plant hormone crosstalk coordinates a sophisticated plant hormone network to achieve specific physiological functions, on both a spatial and temporal level. Thus, the study of hormone–hormone interactions is a competitive field of research for deciphering the underlying regulatory mechanisms. Among plant hormones, ABA and ethylene present a fascinating case of interaction. They are commonly recognized to act antagonistically in the control of plant growth, and development, as well as under stress conditions. However, several studies on ABA and ethylene suggest that they can operate in parallel or even interact positively. Here, an overview is provided of the current knowledge on ABA and ethylene interaction, focusing on abiotic stress conditions and a simplified hypothetical model describing stomatal closure / opening, regulated by ABA and ethylene.

Several experimental evidences have shown that the human endogenous hormones can interact with drugs in many ways and affect drug efficacy. The hormone drug interactions (HDI) are essential for drug treatment and precision medicine; therefore, it is essential to understand the hormone-drug associations. Here, we present HormoNet to predict the HDI pairs and their risk level by integrating features derived from hormone and drug target proteins. To the best of our knowledge, this is one of the first attempts to employ deep learning approach for prediction of HDI prediction. Amino acid composition and pseudo amino acid composition were applied to represent target information using 30 physicochemical and conformational properties of the proteins. To handle the imbalance problem in the data, we applied synthetic minority over-sampling technique technique. Additionally, we constructed novel datasets for HDI prediction and the risk level of their interaction. HormoNet achieved high performance on our constructed hormone-drug benchmark datasets. The results provide insights into the understanding of the relationship between hormone and a drug, and indicate the potential benefit of reducing risk levels of interactions in designing more effective therapies for patients in drug treatments. Our benchmark datasets and the source codes for HormoNet are available in: https://github.com/EmamiNeda/HormoNet .

Following the discovery of leptin in 1994, the scientific and clinical communities have held great hope that manipulation of the leptin axis may lead to the successful treatment of obesity. This hope is not yet dashed; however the role of the leptin axis is now being shown to be ever more complex than was first envisaged. It is now well established that leptin interacts with pathways in the central nervous system and through direct peripheral mechanisms. In this review, we consider the tissues in which leptin is synthesized and the mechanisms which mediate leptin synthesis, the structure of leptin and the knowledge gained from cloning leptin genes in aiding our understanding of the role of leptin in the periphery. The discoveries of expression of leptin receptor isotypes in a wide range of tissues in the body have encouraged investigation of leptin interactions in the periphery. Many of these interactions appear to be direct, however many are also centrally mediated. Discovery of the relative importance of the centrally mediated and peripheral interactions of leptin under different physiological states and the variations between species is beginning to show the complexity of the leptin axis. Leptin appears to have a range of roles as a growth factor in a range of cell types: as be a mediator of energy expenditure; as a permissive factor for puberty; as a signal of metabolic status and modulation between the foetus and the maternal metabolism; and perhaps importantly in all of these interactions, to also interact with other hormonal mediators and regulators of energy status and metabolism such as insulin, glucagon, the insulin-like growth factors, growth hormone and glucocorticoids. Surely, more interactions are yet to be discovered. Leptin appears to act as an endocrine and a paracrine factor and perhaps also as an autocrine factor. Although the complexity of the leptin axis indicates that it is unlikely that effective treatments for obesity will be simply derived, our improving knowledge and understanding of these complex interactions may point the way to the underlying physiology which predisposes some individuals to apparently unregulated weight gain.

Fruit growth and ripening are controlled by multiple phytohormones. How these hormones coordinate and interact with each other to control these processes at the molecular level is unclear. We found in the early stages of Fragaria vesca (woodland strawberry) fruit development, auxin increases both widths and lengths of fruits, while gibberellin [gibberellic acid (GA)] mainly promotes their longitudinal elongation. Auxin promoted GA biosynthesis and signaling by activating GA biosynthetic and signaling genes, suggesting auxin function is partially dependent on GA function. To prevent the repressive effect of abscisic acid (ABA) on fruit growth, auxin and GA suppressed ABA accumulation during early fruit development by activating the expression of FveCYP707A4a encoding cytochrome P450 monooxygenase that catalyzes ABA catabolism. At the onset of fruit ripening, both auxin and GA levels decreased, leading to a steep increase in the endogenous level of ABA that drives fruit ripening. ABA repressed the expression of FveCYP707A4a but promoted that of FveNCED, a rate-limiting step in ABA biosynthesis. Accordingly, altering FveCYP707A4a expression changed the endogenous ABA levels and affected FveNCED expression. Hence, ABA catabolism and biosynthesis are tightly linked by feedback and feedforward loops to limit ABA contents for fruit growth and to quickly increase ABA contents for the onset of fruit ripening. These results indicate that FveCYP707A4a not only regulates ABA accumulation but also provides a hub to coordinate fruit size and ripening times by relaying auxin, GA, and ABA signals.

It is generally not known that most commercial rodent diets are formulated with soy protein and deliver large daily doses of isoflavones to animals throughout their lifespan, including the in utero period. Here, we demonstrate that isoflavones are bioavailable and show that commercial rodent diets universally used by animal facilities lead to very high steady-state serum isoflavone concentrations in adult rats (2613 ± 873 ng/mL) and mice (2338 ± 531 ng/mL), exceeding the animal's endogenous estrogen level by 30,000- to 60,000-fold. We demonstrate the maternal-fetal intrauterine transfer of isoflavones in animals fed a standard Purina 5001 soy-containing diet and show that newborn rat pups have high serum isoflavones levels (540 ± 174 ng/mL) that are maintained throughout the suckling period by passage of isoflavones into maternal milk. These findings have profound implications for all animal experiments, including multigenerational studies and studies of transgenic animals, especially if biochemical or morphological end-points are influenced by the hormonal or nonhormonal properties of phytoestrogens. These compounds have the potential to modulate genotypic and phenotypic expression in general, and therefore, all investigators should be vigilant to the phytoestrogen composition of commercial rodent diets because there is a history of potent biological effects in larger animals and in humans from high circulating isoflavone concentrations.

Controlling energy homeostasis involves modulating the desire to eat and regulating energy expenditure. The controlling machinery includes a complex interplay of hormones secreted at various peripheral endocrine endpoints, such as the gastrointestinal tract, the adipose tissue, thyroid gland and thyroid hormone-exporting organs, the ovary and the pancreas, and, last but not least, the brain itself. The peripheral hormones that are the focus of the present review (ghrelin, leptin, thyroid hormones, oestrogen and insulin) play integrated regulatory roles in and provide feedback information on the nutritional and energetic status of the body. As peripheral signals, these hormones modulate central pathways in the brain, including the hypothalamus, to influence food intake, energy expenditure and to maintain energy homeostasis. Since the growth of the literature on the role of various hormones in the regulation of energy homeostasis shows a remarkable and dynamic expansion, it is now becoming increasingly difficult to understand the individual and interactive roles of hormonal mechanisms in their true complexity. Therefore, our goal is to review, in the context of general physiology, the roles of the five best-known peripheral trophic hormones (ghrelin, leptin, thyroid hormones, oestrogen and insulin, respectively) and discuss their interactions in the hypothalamic regulation of food intake.

Fruit ripening involves the dynamic interaction of phytohormones. Ethylene (ET) and gibberellin (GA) antagonistically affect fruit ripening. However, the mechanism of GA and its potential interaction with ET during fruit ripening remain unknown. To identify the potential molecular mechanism of ET and GA interplay in tomato ( Solanum lycopersicum L.) fruit ripening, transcriptome and metabolomic profiling was carried out in tomato fruit treated with GA, ET or the combination of the two hormones (GA+ET). ET accelerated fruit ripening with the simultaneous repression of auxin signaling. In contrast, gibberellin delayed ripening by the upregulation of auxin signaling. ET signaling and response was inhibited by GA or combined with ET. At the metabolite level, while GA treatment inhibited metabolite shift during ripening, ET treatment promoted. In the combined hormone treatment, ET reduced or recovered GA inhibitory effect on specific metabolites. This study provided insight into ET and GA interaction, highlighting the importance of auxin signaling in metabolic shifts during tomato ripening progression.

Currently, the field of postharvest technology is a growing research area of particular interest since the increase in world population and the need to satisfy its nutritional requirements. These aspects establish a demand to produce fruits with high market quality while minimizing the losses from production to consumption stages. In the past few years, nitric oxide (NO) has emerged as a novel gasotransmitter to improve fruit postharvest shelf-life, owing to its influence on physiological processes (including fruit ripening) and on acclimation responses to stress conditions. In this review, we summarize some of the research related to the effects of NO exposure on different fruits with the aim to extend postharvest shelf-life and quality. The protection against chilling injury and postharvest diseases are addressed. The mechanisms of NO action and its interactions with other phytohormones are analyzed. Finally, the potential use of NO donors (and other strategies destined to enhance its levels) with a technological scope is also discussed.

Recent studies on insulin, leptin, osteocalcin (OCN), and bone remodeling have evoked interest in the interdependence of bone formation and energy household. Accordingly, this study attempts to investigate trauma specific hormone changes in a murine trauma model and its influence on fracture healing. Thereunto 120 female wild type (WT) and leptin-deficient mice underwent either long bone fracture (Fx), traumatic brain injury (TBI), combined trauma (Combined), or neither of it and therefore served as controls (C). Blood samples were taken weekly after trauma and analyzed for insulin and OCN concentrations. Here, WT-mice with Fx and, moreover, with combined trauma showed a greater change in posttraumatic insulin and OCN levels than mice with TBI alone. In the case of leptin-deficiency, insulin changes were still increased after bony lesion, but the posttraumatic OCN was no longer trauma specific. Four weeks after trauma, hormone levels recovered to normal/basal line level in both mouse strains. Thus, WT- and leptin-deficient mice show a trauma specific hyperinsulinaemic stress reaction leading to a reduction in OCN synthesis and release. In WT-mice, this causes a disinhibition and acceleration of fracture healing after combined trauma. In leptin-deficiency, posttraumatic OCN changes are no longer specific and fracture healing is impaired regardless of the preceding trauma.