Class Of Hormones Research Articles

New insights into the regulation of plant immunity by amino acid metabolic pathways

Besides defence pathways regulated by classical stress hormones, distinct amino acid metabolic pathways constitute integral parts of the plant immune system. Mutations in several genes involved in Asp-derived amino acid biosynthetic pathways can have profound impact on plant resistance to specific pathogen types. For instance, amino acid imbalances associated with homoserine or threonine accumulation elevate plant immunity to oomycete pathogens but not to pathogenic fungi or bacteria. The catabolism of Lys produces the immune signal pipecolic acid (Pip), a cyclic, non-protein amino acid. Pip amplifies plant defence responses and acts as a critical regulator of plant systemic acquired resistance, defence priming and local resistance to bacterial pathogens. Asp-derived pyridine nucleotides influence both pre- and post-invasion immunity, and the catabolism of branched chain amino acids appears to affect plant resistance to distinct pathogen classes by modulating crosstalk of salicylic acid- and jasmonic acid-regulated defence pathways. It also emerges that, besides polyamine oxidation and NADPH oxidase, Pro metabolism is involved in the oxidative burst and the hypersensitive response associated with avirulent pathogen recognition. Moreover, the acylation of amino acids can control plant resistance to pathogens and pests by the formation of protective plant metabolites or by the modulation of plant hormone activity.

Genomic and post-genomic leads toward regulation of spermatogenesis

Declining male fertility without sign of any recovery and limited understanding about mechanisms involved in the intra-testicular regulation of spermatogenesis, withholding clinicians from delivering appropriate line of treatment, are serious causes of concern. Several infertile men are not amenable to treatment because hormonal deficiency or physical obstruction is not the underlying cause. A hope has been generated in the post genomic era where we can have information about the testicular genes and proteins which regulate germ cell division, differentiation and maturation in an interactive manner. Expression of some of these genes and proteins may be governed by classical hormones. However, if the genes are defective (naturally or acquired later in life), mere treatment with hormone(s), as is opted presently by clinicians, would not result into production of sperm. High throughput techniques and post genomic endeavors have generated plethora of data for fundamental and clinical andrology. Appropriate analyses and interlinking of these datasets may provide access to very precise information on a myriad of somatic and germ cell specific genes and proteins. Studies of functional genomics involving cell and age specific expression of some of these testicular genes will not only pin point precise role of certain biomolecules in various steps of spermatogenesis but it will also provide strong basis for the diagnosis and treatment of male infertility. In this review, we present some transcriptomic and proteomic information from various testicular somatic and germ cell studies and discuss how a systems biology approach may be brought in to meaningfully utilize the available information.

A Robust and Sensitive Synthetic Sensor to Monitor the Transcriptional Output of the Cytokinin Signaling Network in Planta

Cytokinins are classic plant hormones that orchestrate plant growth, development, and physiology. They affect gene expression in target cells by activating a multistep phosphorelay network. Type-B response regulators, acting as transcriptional activators, mediate the final step in the signaling cascade. Previously, we have introduced a synthetic reporter, Two Component signaling Sensor (TCS)::green fluorescent protein (GFP), which reflects the transcriptional activity of type-B response regulators. TCS::GFP was instrumental in uncovering roles of cytokinin and deepening our understanding of existing functions. However, TCS-mediated expression of reporters is weak in some developmental contexts where cytokinin signaling has a documented role, such as in the shoot apical meristem or in the vasculature of Arabidopsis (Arabidopsis thaliana). We also observed that GFP expression becomes rapidly silenced in TCS::GFP transgenic plants. Here, we present an improved version of the reporter, TCS new (TCSn), which, compared with TCS, is more sensitive to phosphorelay signaling in Arabidopsis and maize (Zea mays) cellular assays while retaining its specificity. Transgenic Arabidopsis TCSn::GFP plants exhibit strong and dynamic GFP expression patterns consistent with known cytokinin functions. In addition, GFP expression has been stable over generations, allowing for crosses with different genetic backgrounds. Thus, TCSn represents a significant improvement to report the transcriptional output profile of phosphorelay signaling networks in Arabidopsis, maize, and likely other plants that display common response regulator DNA-binding specificities.

Regulation of Arabidopsis root development by small signaling peptides

Plant root systems arise de novo from a single embryonic root. Complex and highly coordinated developmental networks are required to ensure the formation of lateral organs maximizes plant fitness. The Arabidopsis root is well-suited to dissection of regulatory and developmental networks due to its highly ordered, predictable structure. A myriad of regulatory signaling networks control the development of plant roots, from the classical hormones such as auxin and cytokinin to short-range positional signaling molecules that relay information between neighboring cells. Small signaling peptides are a growing class of regulatory molecules involved in many aspects of root development including meristem maintenance, the gravitropic response, lateral root development, and vascular formation. Here, recent findings on the roles of regulatory peptides in these aspects of root development are discussed.

Hormone Signaling Networks Open Multiple Routes for Immunity and Disease in Plants

Plant hormones are small signaling molecules that regulate almost every aspect of plant life cycle. Plant pathogens alter hormonal balance of the host to cause disease. In response, host redefines hormone signaling networks to cope with the invading pathogen. Biotrophic pathogens are generally sensitive to salicylic acid mediated defense responses, whereas necrotrophic pathogens are deterred through jasmonate/ethylene pathways. Interaction between these pathways is regarded as central backbone of plant immunity. Classic hormones such as auxin, gibberellin, and cytokinin either promote salicylic acid or jasmonates mediated networks of immunity in plants. Here, we advocate a network biology perspective and emphasize the application of systems biology approaches for a comprehensive understanding of plantpathogen interactions.

English

For citation purposes: Laurentino S, Pinto P, Correia S, Cavaco JE, Canario AVM, Socorro S. Structural variants of sex steroid hormone receptors in the testis: from molecular biology to physiological roles. OA Biotechnology 2012 Dec 17;1(2):4. Licensee OA Publishing London 2012. Creative Commons Attribution License (CC-BY) Abstract Introduction Sex steroid hormones, androgens and oestrogens regulate diverse physiological processes by interacting with their intracellular protein receptors and modulating the expression of target genes. Classical sex steroid hormone receptors belong to the nuclear receptor superfamily, which forms the largest known family of transcription factors in eukaryotes. A common feature of sex steroid hormone receptors genes is the incidence of alternative splicing, a process that generates multiple variants from a single mRNA precursor molecule. This process facilitates the production of functionally distinct proteins and contributes to proteome diversity in higher eukaryotes. Herein we will critically review current information about the diversity of oestrogen receptors and androgen receptors variants, discussing their structural features and physiological functions. Conclusion The identification of structural variants of both ERs and ARs in healthy testis and a broad range of vertebrate species, highlights the newly revealed complexity of SSHRs signalling mechanisms in this tissue. Structural variants of sex steroid hormone receptors in the testis: from molecular biology to physiological roles

Fragmentation pathway studies of several plant hormones using an electrospray ionization-quadrupole/time-of-flight mass spectrometer

Auxins, cytokinins (CKs), gibberellins (GAs), and abscisic acid (ABA) are four classes of plant hormones, which play important roles in phytophysiology. However, few mass spectrometric fragmentation pathway studies of these compounds have been performed using a high-resolution mass spectrometer. Therefore, there is an urgent need to research the fragmentation pathways of classic plant hormones. In this study, the fragmentation pathways of four types of plant hormones were studied by employing an electrospray ionization-quadrupole/time-of-flight (ESI-Q/TOF) mass spectrometer. The accurate masses of the ions in the mass spectrometer (MS) and the product ions in the MS/MS were combined and used to obtain the MS fragmentation pathways of these compounds. The exact mass-to-charge ratio for each product ion was determined to deduce the elemental compositions for each compound. Most of the ions were assigned according to the collected high-resolution accurate mass data, and typical fragmentation pathways of the four classes of plant hormones were proposed. Furthermore, a comprehensive MS/MS spectra library of the plant hormones was established for the first time using ESI-Q/TOF. For instance, a characteristic mass signal of m/z 130 was identified for the product ions of the indole 3-acetic acid homologue auxins in the positive ion mode and for the characteristic neutral loss of CO2CO2H2O for gibberellin in the negative ion mode. These findings are valuable for the identification of a variety of plant hormones and could also provide a basis for developing MS-based methods of detecting or screening a target class of plant hormones in plant extracts.

Hormonal regulation of phosphate balance

Phosphate homeostasis is maintained by intestine, bone, and kidney, which is regulated by many hormones. In addition to classical hormones such as parathyroid hormone (PTH) and 1,25-dihydroxyvitamin D [1,25 (OH) (2)D] , fibroblast growth factor 23 (FGF23) and Klotho have been discovered as novel factors for phosphate metabolism. FGF23 is a circulating hormone that is synthesized by osteocytes and osteoblasts in bone. The physiological actions of FGF23 are to promote phosphaturia and decrease production of 1,25 (OH) (2)D. Klotho was initially identified as an anti-aging protein, but subsequent research revealed multiple functions of Klotho in phosphate metabolism. Klotho directly binds to FGF receptor 1 (FGFR1) and contributes to FGFR1-Klotho complex-mediated signal transduction with higher affinity than FGFR1 or Klotho alone. In addition, the extracellular domain of Klotho is clipped by enzymes and secreted into blood, which exerts phosphaturic effects independently of FGF23. In the regulation of phosphate metabolism, this FGF23-Klotho axis constitutes feedback loops with classical factors such as PTH and 1,25 (OH) (2)D. However, the precise feedback system in the phosphate metabolism remains to be determined and further research is required to provide a greater understanding of the phosphate metabolism system.

Defence on demand: mechanisms behind optimal defence patterns

The optimal defence hypothesis (ODH) predicts that tissues that contribute most to a plant's fitness and have the highest probability of being attacked will be the parts best defended against biotic threats, including herbivores. In general, young sink tissues and reproductive structures show stronger induced defence responses after attack from pathogens and herbivores and contain higher basal levels of specialized defensive metabolites than other plant parts. However, the underlying physiological mechanisms responsible for these developmentally regulated defence patterns remain unknown. This review summarizes current knowledge about optimal defence patterns in above- and below-ground plant tissues, including information on basal and induced defence metabolite accumulation, defensive structures and their regulation by jasmonic acid (JA). Physiological regulations underlying developmental differences of tissues with contrasting defence patterns are highlighted, with a special focus on the role of classical plant growth hormones, including auxins, cytokinins, gibberellins and brassinosteroids, and their interactions with the JA pathway. By synthesizing recent findings about the dual roles of these growth hormones in plant development and defence responses, this review aims to provide a framework for new discoveries on the molecular basis of patterns predicted by the ODH. Almost four decades after its formulation, we are just beginning to understand the underlying molecular mechanisms responsible for the patterns of defence allocation predicted by the ODH. A requirement for future advances will be to understand how developmental and defence processes are integrated.

Expression of the G protein-coupled estrogen receptor (GPER) in endometriosis: a tissue microarray study

BackgroundThe G protein-coupled estrogen receptor (GPER) is thought to be involved in non-genomic estrogen responses as well as processes such as cell proliferation and migration. In this study, we analyzed GPER expression patterns from endometriosis samples and normal endometrial tissue samples and compared these expression profiles to those of the classical sex hormone receptors.MethodsA tissue microarray, which included 74 samples from different types of endometriosis (27 ovarian, 19 peritoneal and 28 deep-infiltrating) and 30 samples from normal endometrial tissue, was used to compare the expression levels of the GPER, estrogen receptor (ER)-alpha, ER-beta and progesterone receptor (PR). The immunoreactive score (IRS) was calculated separately for epithelium and stroma as the product of the staining intensity and the percentage of positive cells. The expression levels of the hormonal receptors were dichotomized into low (IRS < 6) and high (IRS > =6) expression groups.ResultsThe mean epithelial IRS (+/−standard deviation, range) of cytoplasmic GPER expression was 1.2 (+/−1.7, 0–4) in normal endometrium and 5.1 (+/−3.5, 0–12) in endometriosis (p < 0.001), of nuclear GPER 6.4 (+/−2.6, 0–12) and 6.8 (+/−2.9, 2–12; p = 0.71), of ER-alpha 10.6 (+/−2.4, 3–12) and 9.8 (+/−3.0, 2–12; p = 0.26), of ER-beta 2.4 (+/−2.2; 0–8) and 5.6 (+/−2.6; 0–10; p < 0.001), and of PR 11.5 (+/−1.7; 3–12) and 8.1 (+/−4.5; 0–12; p < 0.001), respectively. The mean stromal IRS of nuclear GPER expression was 7.7 (+/−3.0; 2–12) in endometrium and 10.8 (+/−1.7; 6–12) in endometriosis (p < 0.001), of ER-alpha 8.7 (+/−3.1; 2–12) and 10.6 (+/−2.4; 2–12; p = 0.001), of ER-beta 1.8 (+/−2.0; 0–8) and 5.4 (+/−2.5; 0–10; p < 0.001), and of PR 11.7 (+/−0.9; 8–12) and 10.9 (+/−2.0; 3–12; p = 0.044), respectively. Cytoplasmic GPER expression was not detectable in the stroma of endometrium and endometriosis. The observed frequency of high epithelial cytoplasmic GPER expression levels was 50% (n = 30/60) in the endometriosis and none (0/30) in the normal endometrium samples (p < 0.001). High epithelial cytoplasmic GPER expression levels were more frequent in endometriomas (14/20, 70%; p = 0.01), as compared to peritoneal (9/18, 50%) or deep-infiltrating endometriotic lesions (7/22, 31.8%). The frequency of high stromal nuclear GPER expression levels was 100% (n = 74/74) in endometriosis and 76.7% (n = 23/30) in normal endometrium (p < 0.001). The frequency of high epithelial nuclear GPER expression levels did not differ between endometriosis and normal endometrium.ConclusionsThe present data indicate a unique GPER expression pattern in endometriosis, especially in endometriomas as compared to the normal endometrium. The overexpression of GPER in endometriotic lesions suggests a potential role for GPER in the hormonal regulation of endometriosis, which should be taken into consideration for future hormonal treatment strategies.

Expression of Chemokine CXCL12 and Its Receptor CXCR4 in Folliculostellate (FS) Cells of the Rat Anterior Pituitary Gland: The CXCL12/CXCR4 Axis Induces Interconnection of FS Cells

The anterior pituitary gland is composed of five types of hormone-producing cells plus folliculostellate (FS) cells, which do not produce classical anterior pituitary hormones. FS cells are interconnected by cytoplasmic processes and encircle hormone-producing cells or aggregate homophilically. Using living-cell imaging of primary culture, we recently reported that some FS cells precisely extend their cytoplasmic processes toward other FS cells and form interconnections with them. These phenomena suggest the presence of a chemoattractant factor that facilitates the interconnection. In this study, we attempted to discover the factor that induces interconnection of FS cells and succeeded in identifying chemokine (CXC)-L12 and its receptor CXCR4 as potential candidate molecules. CXCL12 is a chemokine of the CXC subfamily. It exerts its effects via CXCR4, a G protein-coupled receptor. The CXCL12/CXCR4 axis is a potent chemoattractant for many types of neural cells. First, we revealed that CXCL12 and CXCR4 are expressed by FS cells in rat anterior pituitary gland. Next, to clarify the function of the CXCL12/CXCR4 axis in FS cells, we observed living anterior pituitary cells in primary culture with specific CXCL12 inhibitor or CXCR4 antagonist and noted that extension of cytoplasmic processes and interconnection of FS cells were inhibited. Finally, we examined FS cell migration and invasion by using Matrigel matrix assays. CXCL12 treatment resulted in markedly increased FS cell migration and invasion. These data suggest that FS cells express chemokine CXCL12 and its receptor CXCR4 and that the CXCL12/CXCR4 axis evokes interconnection of FS cells.

Mini-review: new therapeutic options in hypoparathyroidism

Hypoparathyroidism is a disorder characterized by hypocalcemia and low or absent parathyroid hormone (PTH). While standard treatment of hypoparathyroidism consists of oral calcium and vitamin D supplementation, maintaining serum calcium levels can be a challenge, and concerns exist regarding hypercalciuria and ectopic calcifications that can be associated with such treatment. Hypoparathyroidism is the only classic endocrine deficiency disease for which the missing hormone, PTH, is not yet an approved treatment. This mini-review focuses on the use of PTH in the treatment of hypoparathyroidism. There are two available formulations of PTH: teriparatide [human PTH(1-34)] and the full-length molecule, PTH(1-84). Both PTH(1-34) and PTH(1-84) lower supplemental vitamin D requirements and increase markers of bone turnover. Densitometric and histomorphometric studies in some subjects treated with PTH(1-84) demonstrate improvement in abnormal bone-remodeling dynamics and return of bone metabolism toward normal euparathyroid levels. Further detailed examination of skeletal features following therapy with the different treatment regimens and data regarding the effect of PTH on quality of life measures are under active investigation.

Dopamine in Immunoregulation

In this issue Toth et al. [1] discusses the role of peripheral and brain derived dopamine (DA) in immune regulation. Here we consider briefly the possible way by which hormones and other central regulatory factors act peripherally in vivo. During the early years of the nineteenth centaury Endocrinologists recognized first when searching for the origin of hormones, that “everything is made everywhere”. This rule was true for all hormones and neurotransmitters that have been examined. This phenomenon has been re-discovered since that time over and over again. DA exerts an inhibitory effect on prolactin (PRL) and growth hormone (GH) secretion. This effect is very powerful. In rats treatment with bromocriptine (a DA agonist drug), inhibited completely the adaptive immune function (ADIM) [2]. The rule in the Neuroimmune Supersystem [3] is that mediators are shared: so classical hormones and neuropeptides are made in the immune system and everywhere else, lymphokines were discovered in the immune system first, but then were found in many other tissues and cells so their name was changed to cytokines, which implies tissue hormones. Sharing makes communication instantaneously possible [3]. Dopamine is no exception to this rule. It is made in the central nervous system (CNS) but also in various cell types in the immune system, and in many other tissue and organs in the body. In short, dopamine is made everywhere and acts everywhere [1]. One may argue that dopamine is a powerful immunoregulator, it can act centrally by inhibiting PRL secretion, and also acts peripherally by paracrine/autocrine (P/A) regulation. Yes indeed, this is very important from the point of usefulness. But how the central and peripheral mechanisms work under homeostatic conditions? There are myriads of mediators produced centrally, peripherally, and receptors are expressed and may be activated everywhere. This may lead to a very chaotic situation, signals are delivered everywhere; cells could go crazy under such bombarding. It was proposed that membrane bound receptors will cap on one pole of the cell surface after activation by specific ligands. Such receptors are phosphorylated by protein kinases and de-phoshorylated by phosphatases, which happens competitively at the same time. If phosphorylation is stronger the cell will be activated, if de-phosphorylation is stronger, the cells will be inhibited [4]. But there are many other mediators that do not use this signal transmission pathway. Alternate mechanisms are used by some membrane receptors. Also, there are cytoplasmic and nuclear receptors, which definitely would not be controlled by this kind of regulation [5]. It is important that every regulatory circuit has positive and negative signals and the signals will balance out physiologically, possibly under CNS control. The fact is that in spite of the countless mediators, receptors and signaling, the organism remains normal, all functions are in harmony and in homeostasis. The classical answer is that the CNS controls everything, so the peripheral mechanisms are kept under control by the CNS. Indeed we observed that PRL production by lymphocytes was regulated by the pituitary gland [6]. This would suggest that the CNS might exert a regulatory influence on all regulatory circuits under normal, homeostatic conditions. Could DA of CNS origin signal the immune system or other systems, tissues directly? The answer is yes. Dopaminergic nerves deliver DA to the tissues for local use. Apparently the CNS is in control here again. So it seems that during homeostasis, the local consumption of DA may be CNS regulated [1]. During homeostasis, cytokines are at minimal or undetectable level in the serum. During acute febrile illness cytokines of innate immunity (INIM) origin [e.g. interleukin – (IL1)-beta, IL-6, and tumor

New insights into the signaling and function of cytokinins in higher plants

Phytohormones (plant hormones) play a role in the regulation of cellular activities including cell division, elongation and differentiation, pattern formation, organogenesis, reproduction, sex determination, and responses to abiotic and biotic stress. The phytohormonal signal transduction pathways operate via cytokinin perception by transmembrane receptors consisting of two domains: an extracellular domain responsible for hormone binding and an intracellular domain, sensory His / Asp kinase (HK). Upon phytohormone binding, the receptor undergoes a conformational change which activates its protein kinase activity. The phosphorylated intracellular domain transfers the phosphoryl group to the His residue of the histidine phosphotransfer protein (HPt) which in turn phosphorylates Asp residue in the Response Regulator (RR). The phosphorylated RR protein acts as either a positive or negative transcription factor that interacts with the gene promoter or other target protein. The two-component signaling pathway, operating through the His-Asp phosphorelay, controls many physiological and developmental processes throughout the plant lifecycle (from seed-to-seed). Downstream plant hormone signaling also includes proteolysis of transcriptional regulators that block the activity of transcription factors. Two-component signaling operates more frequently in higher plants. Five classic plant hormones had been discovered by the middle of the twentieth century: auxins, cytokinins, gibberellins, ethylene and abscisic acid. The more recently characterized hormones include brassinosteroids, strigolactones, jasmonates and salicylates. Considering the tremendous work that has been undertaken during the last decades, in this review we decided to concentrate on cytokinin signaling in various plant developmental processes, including responses to biotic and abiotic stresses.

Safety, Efficacy and Patient Acceptability of Bazedoxifene Acetate in the Management of Postmenopausal Osteoporosis

Many pharmacological agents are available for treatment of postmenopausal osteoporosis, including estrogen and the selective modulators of estrogen receptor (SERMS). Bazedoxifene is a third-generation SERM, which acts as estrogen agonist in bone and lipid metabolism and as an antagonist in the breast and endometrium. Studies demonstrated that bazedoxifene reduced significantly the risk of vertebral fractures. In a subgroup of patients at high risk (post-hoc analysis), a reduction of nonvertebral fractures risk was reported. Moreover, the combination of conjugated estrogens with bazedoxifene seems to offer an alternative to classical hormone therapy, improving the vasomotor symptoms and vaginal atrophy, without the use of a progestin. Bazedoxifene is a promising drug for the treatment and prevention of osteoporosis in postmenopausal women; however a safety concern regarding venous thromboembolic events is needed before starting treatment.

P4-02-09: Estrogen-Related Receptor a Mediates Insulin-Like Growth Factor-I Dependent Migration in Breast Cancer Cells.

Abstract The orphan nuclear estrogen-related receptors (ERR) have homology to steroid hormone receptors. Unlike classical steroid hormone receptors, ERRs do not have known ligands but are transcriptionally activated upon binding to nuclear receptor coregulators such as PGC1α, PGC1β, and PPRC1. ERRs regulate energy metabolism and are accordingly expressed in tissues that require high energy production. ERRs recognize their own ERRE (estrogen-related receptor response element) gene promoters, but can also activate transcription via ERE (estrogen receptor response element) promoters, representing the ability of ERRs to cross participate in ERα regulatory pathways in the absence of estrogen. Of the three family members (α,β,γ), ERRα is the most highly expressed in breast tissue. ERRα expression was found to be increased in ERα negative breast cancers and associated with poor prognoses. ERRα and its coactivators can increase the expression of a critical mediator of breast tumor angiogenesis and metastasis, VEGFA. We have previously shown that VEGFA is regulated by insulin and IGF receptor activation and hypothesized that ERRα may be a mediator of this finding. We therefore explored whether ERRα and its coactivators are necessary for IGF-I/insulin dependent regulation of VEGFA and cell migration. ERRα was expressed in breast cancer cell lines, but no correlation was observed with breast cancer subtypes. Reducing endogenous ERRα levels by shRNA reduced IGF-I dependent migration in MDA-MB-231 cells. These results were confirmed using an ERRα specific inverse agonist (XCT-790), which also inhibited MDA-MB-231 cell migration. Modulating ERRα mRNA levels via shRNA resulted in decreased VEGFA mRNA levels in MCF7L cells and increased VEGFA mRNA levels in MDA-MB-231 cells, while the inverse agonist XCT-790 caused an increase in VEGFA mRNA levels in both cell lines. Reducing ERRa levels did not affect the expression of the IGF1R, InsR, IRS-1, IRS-2, PI-3K-Akt-mTOR dependent signaling pathway. Neither ERRα protein nor mRNA levels were modulated by IGF-I or insulin. We conclude that ERRα is important for mediating IGF-I dependent migration, but have shown that ERRα is not directly regulated by the IGF signaling. We will next explore the role of ERRα's coregulators (PGC1α, PGC1β, and PPRC1) in the regulation of VEGFA by the IGF/insulin pathway given their central role in regulating ERRα's function. Citation Information: Cancer Res 2011;71(24 Suppl):Abstract nr P4-02-09.

Ethylene-responsive miRNAs in roots of Medicago truncatula identified by high-throughput sequencing at whole genome level

Ethylene is one of the classical plant hormones with a diverse function in plant growth and development. Root elongation is sensitive to ethylene such that treatments with ethylene and the ethylene precursor 1-aminocyclopropane-1-carboxylic acid (ACC) inhibit root growth. MicroRNA as one type of endogenous, non-coding small RNAs, plays an important role in regulation of plant growth, development and hormonal signaling by affecting expression of target genes. However, there has been no detailed study to evaluate the role of microRNAs in mediation of ethylene-dependent physiological processes in plants. Medicago truncatula is a model plant widely used for investigation of molecular biology in legume species. In this study, we constructed two small RNA libraries from roots of M. truncatula treated with and without ACC. High-throughput sequencing was employed to sequence the small RNA libraries, and more than 30M raw reads were obtained. We annotated 301 known miRNAs and identified 3 new miRNAs in the two libraries. Treatment of M. truncatula with 10μM ACC led to changes in expression of 8 miRNAs. The targets of the ethylene-responsive miRNAs were predicted by bioinformatic approach. The potential role of the ethylene-responsive miRNAs in the ethylene-induced inhibition of root elongation is discussed. These results are useful for functional characterization of miRNAs in mediation of ethylene-dependent physiological processes in general and root elongation in particular.

Structural basis for cytokinin recognition by Arabidopsis thaliana histidine kinase 4

Cytokinins are classic plant hormones that orchestrate growth, development and the integrity of stem cell populations. Cytokinin receptors are eukaryotic sensor histidine kinases that are activated both by naturally occurring adenine-type cytokinins and by urea-based synthetic compounds. Crystal structures of the Arabidopsis histidine kinase 4 sensor domain in complex with different cytokinin ligands now rationalize the hormone-binding specificity of the receptor and may spur the design of novel cytokinin ligands.

Hormone Crosstalk in Plant Disease and Defense: More Than Just JASMONATE-SALICYLATE Antagonism

Until recently, most studies on the role of hormones in plant-pathogen interactions focused on salicylic acid (SA), jasmonic acid (JA), and ethylene (ET). It is now clear that pathogen-induced modulation of signaling via other hormones contributes to virulence. A picture is emerging of complex crosstalk and induced hormonal changes that modulate disease and resistance, with outcomes dependent on pathogen lifestyles and the genetic constitution of the host. Recent progress has revealed intriguing similarities between hormone signaling mechanisms, with gene induction responses often achieved by derepression. Here, we report on recent advances, updating current knowledge on classical defense hormones SA, JA, and ET, and the roles of auxin, abscisic acid (ABA), cytokinins (CKs), and brassinosteroids in molding plant-pathogen interactions. We highlight an emerging theme that positive and negative regulators of these disparate hormone signaling pathways are crucial regulatory targets of hormonal crosstalk in disease and defense.

Molecules important for thyroid hormone synthesis and action - known facts and future perspectives

Thyroid hormones are of crucial importance for the functioning of nearly every organ. Remarkably, disturbances of thyroid hormone synthesis and function are among the most common endocrine disorders affecting approximately one third of the working German population. Over the last ten years our understanding of biosynthesis and functioning of these hormones has increased tremendously. This includes the identification of proteins involved in thyroid hormone biosynthesis like Thox2 and Dehal where mutations in these genes are responsible for certain degrees of hypothyroidism. One of the most important findings was the identification of a specific transporter for triiodothyronine (T3), the monocarboxylate transporter 8 (MCT8) responsible for directed transport of T3 into target cells and for export of thyroid hormones out of thyroid epithelial cells. Genetic disturbances of MCT8 in patients result in a biochemical constellation of high T3 levels in combination with low or normal TSH and thyroxine levels leading to a new syndrome of severe X-linked mental retardation. Importantly mice lacking MCT8 presented only with a mild phenotype, indicating that compensatory mechanisms exist in mice. Moreover, it has become clear that not only genomic actions of T3 exist. T3 is also capable to activate adhesion receptors and it signals via activation of PI3K and MAPK pathways. Most recently, thyroid hormone derivatives were identified, the thyronamines which are decarboxylated thyroid hormones initiating physiological actions like lowering body temperature and heart rate, thereby acting in opposite direction to the classical thyroid hormones. So far it is believed that thyronamines function via the activation of a G-protein coupled receptor, TAAR1. The objective of this review is to summarise the recent findings in thyroid hormone synthesis and action and to discuss their implications for diagnosis of thyroid disease and for treatment of patients.