Signaling pathways of heat- and hypersalinity-induced polyp bailout in Pocillopora acuta

Polyp bailout is a drastic response to acute stress where coral coloniality breaks down and polyps detach. We induced polyp bailout in Pocillopora acuta with heat stress and tested for differential gene expression using RNAseq and a qPCR assay. Furthermore, we induced polyp bailout with hypersalinity and compared the results to identify stressor-independent signals and pathways active during polyp bailout. Both stressors led to the onset of polyp bailout and the detachment of vital polyps. We observed activation of microbe-associated molecular pattern receptors and downstream signaling pathways of the innate immune system. Further, we detected growth factors and genes active during Wnt-signaling potentially contributing to wound healing, regeneration, and proliferation. Upregulation of several genes encoding for matrix metalloproteinases and the fibroblast growth factor signaling pathway are the most likely involved in the remodeling of the extracellular matrix, as well as in the detachment of polyps from the calcareous skeleton during polyp bailout. Expression of genes of interest in our qPCR assay of vital polyps from our heat-stress experiment, showed a trend for a normalization of gene expression after polyp bailout. Our results provide new insights into the signaling cascades leading to the observed physiological responses during polyp bailout. Comparison between the two stressors showed that certain signaling pathways are independent of the stressor and suggested that polyp bailout is a general response of corals to acute stress. Furthermore, immune system responses during polyp bailout indicate that microbe-associated partners of corals may lead to the polyp bailout response.

     

Unveiling asexual reproductive traits in black corals: polyp bail-out in Antipathella subpinnata

Cnidarians are known to undergo reverse development as a survival mechanism against adverse environmental conditions. Polyp bail-out consists in the polyps’ detachment from the mother colony due to stressful conditions, followed by a complete tissue and cells rearrangement and in some cases in a regression into a simple, ciliated form. Here we describe a massive polyp bail-out event occurred in the mesophotic black coral Antipathella subpinnata in reared conditions. This is the first report of a bail-out event in this species providing new insights into the life cycle and ecology of black corals.

     

Effects of colony size and polyp position on polyp fecundity in the scleractinian coral genus Acropora

This study examined the effects of colony size and polyp position on six variables of polyp fecundity [egg number, egg size, total egg volume, total testis volume, total gonad volume, and gonad ratio (egg volume/testis volume)] in three tabular Acropora corals (Scleractinia), A. hyacinthus, A. japonica, and A. solitaryensis. Samples were collected from various colony sizes (n = 21–30 colonies species^?1), just before the predicted spawning at Kochi, Japan, in 2009. Five replicate polyps were sampled at three positions (center, middle, and outer) from the center to the marginal area in each tabular colony. Results indicated effects of colony size and polyp position on both male and female gonads polyp^?1. A positive effect of colony size was observed on variables of female gonads polyp^?1 (egg number, total egg volume) in A. hyacinthus only, while the positive effect on the variable of male gonads polyp^?1 (total testis volume) was common in all Acropora species, with total testis volume polyp^?1 increasing 2–4-fold from the small (200–400 cm²) to the large size class (5,000–9,000 cm²). Among the polyp positions, lower values were observed mostly in center polyps in A. hyacinthus, while lower values were observed only in outer polyps in the other Acropora species. The distinct patterns between A. hyacinthus and the other two Acropora species suggest different reproductive strategies at the species level. Further studies are needed to confirm the prevalence of these effects in scleractinian corals, which will broaden our understanding of reproductive life history strategies and improve the estimation of reproductive performance.     

Signaling pathways in medulloblastoma

Medulloblastoma is the most common brain tumor of childhood. Multiple signaling pathways have been associated with medulloblastoma formation and growth. These include the developmental pathways Hedgehog, (Hh) Notch, and Wnt as well as the receptor tyrosine kinases (RTK) c-Met, erbB2, IGF-R and TrkC, and the oncoprotein Myc. Here we review the involvement of these pathways in medulloblastoma malignancy with a focus on their mode of deregulation, prognostic value, functional effects, cellular and molecular mechanisms of action, and implications for therapy.     

Signaling pathways in phagocytosis

Phagocytosis is an uptake of large particles governed by the actin-based cytoskeleton. Binding of particles to specific cell surface receptors is the first step of phagocytosis. In higher Eucaryota, the receptors able to mediate phagocytosis are expressed almost exclusively in macrophages, neutrophils, and monocytes, conferring immunodefence properties to these cells. Receptor clustering is thought to occur upon particle binding, that in turn generates a phagocytic signal. Several pathways of phagocytic signal transduction have been identified, including the activation of tyrosine kinases and (or) serine/threonine kinase C in pivotal roles. Kinase activation leads to phosphorylation of the receptors and other proteins, recruited at the sites of phagocytosis. Monomeric GTPases of the Rho and ARF families are likely to be engaged downstream of activated receptors. The GTPases, in cooperation with phosphatidylinositol 4-phosphate 5-kinase and phosphatidylinositol 3-kinase lipid modifying enzymes, can modulate locally the assembly of the submembranous actin filament system leading to particle internalization. BioEssays 21:422–431, 1999. © 1999 John Wiley & Sons, Inc.     

Signaling pathways that regulate Trypanosoma cruzi infection and immune response

Current understanding of key cellular pathways, which are activated by the interaction between T. cruzi and host immunity, is crucial for controlling T. cruzi infection and also for limiting the development of the immunopathological symptoms of Chagas´ disease. Here, we focus on recent advances in the knowledge of modulation of innate receptors such as TLRs and NLRs, especially NLRP3, by T. cruzi in different cells of the immune system. On the other hand, the modulation of macrophage activation may be instrumental in allowing parasite persistence and long-term host survival. In this sense, we discuss the importance of the metabolism of two amino acids: L-arginine and tryptophan, and evaluate the role of iNOS, arginase and IDO enzymes in the regulation of innate and adaptive immune response during this infection; and, finally, we also discuss how T. cruzi exploits the AhR, mTOR and Wnt signaling pathways to promote their intracellular replication in macrophages, thus evading the host's immune response.     

Signaling pathways involved in virulence and stress response of plant-pathogenic Fusarium species

Fungal pathogens face similar stress conditions to those affecting plants and saprotrophic fungi. Therefore, mechanisms underlying fungal response to the stress factors may be well-conserved across various taxa. Saccharomyces cerevisiae was the most researched for signal transduction pathways but many of the pathways' components were later reported for filamentous fungi as well. The most widely studied pathways are those involving the G proteins, adenylate cyclase (cAMP) and mitogen-activated protein kinases (MAPKs). Apart from these, the target-of-rapamycin (TOR), calcium/calcineurin and cell wall integrity (CWI) pathways are of significant interest when stress response is considered. All these pathways were included in this review. It seems that the TOR-received signals are transferred to the CWI pathway, secondary metabolism and virulence. Specific and non-specific cellular responses of Fusarium species, triggered by signals received from the environment, were discussed, with particular focus on stress response and pathogenicity towards the plant host.     

Signaling pathways in elastic tissues

For many years elastin was considered as the matrix component structurally required to provide tissue elasticity. However, the expanded knowledge on the regulation of connective tissue homeostasis has revealed that elastic fibers also represent a source of elastokines and are the target of a number of signaling pathways mainly involving the TGF-β/BMP axis. A better understanding of these complex regulatory networks may pave the way for targeted therapeutic strategies in a number of genetic as well as acquired diseases and for the development of new functionalized biomaterials.     

Signaling pathways regulating gliomagenesis

The astrocytomas represent the most common primary tumors of the brain. Despite efforts to improve the treatment of astrocytomas, these tumors and in particular the high-grade astrocytoma termed glioblastoma multiforme still carry a poor prognosis. In recent years, there has been an intensive effort to gain an understanding of the cellular and molecular mechanisms that contribute to the pathogenesis of astrocytomas as a first step toward the development of better treatments for these devastating tumors. Here, we will review our current understanding of the signaling pathways that underlie glial transformation. Studies of astrocytomas have led to the identification of two major groups of signaling proteins whose abnormalities contribute to gliomagenesis: the cell cycle pathways and the growth factor-regulated signaling pathways. Among the cell cycle proteins, the p16-cdk4-pRb and ARF-MDM2-p53 cell cycle arrest pathways play a prominent role in glial transformation. In addition, deregulation of polypeptide growth factors acting via receptor tyrosine kinases (RTKs) and of intracellular signals, including the lipid phosphatase PTEN, that regulate cellular responses to RTKs plays a critical role in gliomagenesis. In addition to the identification of the signaling proteins targeted in glial transformation, the cell-of-origin of astrocytomas has been investigated. Genetic modeling of astrocytomas in mice suggests that neuroepithelial precursor cells represent preferred cellular substrates of gliomas or that either astrocytes or precursor cells constitute potential cells-of-origin of astrocytomas. During normal brain development, neuroepithelial precursor cells, including neural stem cells, differentiate into astrocytes. As the mechanisms that control gliogenesis during normal brain development become better understood, it will be important to determine if deregulation of these mechanisms might contribute to the pathogenesis of astrocytomas. The elucidation of the molecular underpinnings of astrocytomas holds the promise of improved treatment options for patients with these devastating brain tumors.     

Signaling pathways involved in MDSC regulation

The immune system has evolved mechanisms to protect the host from the deleterious effects of inflammation. The generation of immune suppressive cells like myeloid derived suppressor cells (MDSCs) that can counteract T cell responses represents one such strategy. There is an accumulation of immature myeloid cells or MDSCs in bone marrow (BM) and lymphoid organs under pathological conditions such as cancer. MDSCs represent a population of heterogeneous myeloid cells comprising of macrophages, granulocytes and dendritic cells that are at early stages of development. Although, the precise signaling pathways and molecular mechanisms that lead to MDSC generation and expansion in cancer remains to be elucidated. It is widely believed that perturbation of signaling pathways involved during normal hematopoietic and myeloid development under pathological conditions such as tumorogenesis contributes to the development of suppressive myeloid cells. In this review we discuss the role played by key signaling pathways such as PI3K, Ras, Jak/Stat and TGFb during myeloid development and how their deregulation under pathological conditions can lead to the generation of suppressive myeloid cells or MDSCs. Targeting these pathways should help in elucidating mechanisms that lead to the expansion of MDSCs in cancer and point to methods for eliminating these cells from the tumor microenvironment.     

Signaling pathways in odorant detection.

The application of molecular genetic techniques has led to the identification of olfactory-specific proteins that represent each component in a second messenger cascade. Our current understanding of signaling in the olfactory system suggests that receptor proteins of a large family, responsible in part for the specificity of the system, converge on a relatively small number of second messenger systems. The ability to express these elements in heterologous systems should allow for the reconstitution of the signaling cascade and provide insight into the specificity of ligand binding, pathway activation, and signal termination.     

A new laboratory method for monitoring deep-water coral polyp behaviour

Deep-water corals are found along the oceanic margins world-wide and in the north east Atlantic the most abundant species is Lophelia pertusa (L.). There is now growing evidence that deep-water reefs formed by such species are coming under increasing pressures from resource exploitation, principally deep-sea trawling and hydrocarbon exploration. Here a novel and unobtrusive method of recording deep-water coral behaviour in the laboratory is described using time-lapse video to record silhouettes of the polyps under infrared illumination. The polyps of L. pertusa behaved asynchronously and did not show any clear diurnal patterns over a three-day observation period. Conceptually, sessile benthic suspension feeders appear to be vulnerable to smothering by sediments disturbed by bottom trawls or sub-seabed drilling. This method allows deep-water coral polyp behaviour to be continuously monitored in the laboratory and, therefore, the responses of coral polyps to environmental perturbations such as sedimentation can be recorded. Further work is necessary to resolve the sensitivity of deep-water corals to short-term environmental change and the combined approach of in situ monitoring and subsequent laboratory experimentation has great potential to address these issues.     

Symbiotic pathways of carbon in coral reef ecosystems

Summary 1. Productivity of algal-invertebrate symbiosis in coral reef ecosystems is discussed, and current methods of analysis described.2. Translocation within the symbiosis, apparent rates of turnover, the retention time of carbon fixed in photosynthesis and the excretory pathways leading to the reef community are examined. Possible mechanisms for recycling carbon back to the level of the primary producers are presented.3. Future prospects for in situ studies of the coral reef problem, and the requirements for substantiative data in these areas are discussed.

---

Symbiotische Wege des Kohlenstoffs in Korallenriff-Ökosystemen. Gegenwärtiger Status und zukünftige Aussichten

Kurzfassung Die metabolische Leistungsfähigkeit des Ökosystems Korallenriff basiert zu einem wesentlichen Teil auf der unmittelbaren zellulären Integration von Primärproduzenten und Konsumenten in der symbiotischen Verbindung von Algen und Korallen. Diese Form des Zusammenlebens zweier Organismen stellt ein charakteristisches Merkmal der tropischen Korallenriffe dar und spielt eine Schlüsselrolle bei der Aufrechterhaltung des Ernährungsgleichgewichts innerhalb dieses Ökosystems. Die gegenwärtigen Kenntnisse in bezug auf die Primärproduktion und den Weg des durch die Symbionten fixierten Kohlenstoffs werden besprochen. Methoden für In-situ-Forschungen werden an Hand der bisher erzielten Ergebnisse bewertet, und die Aussichten, die Energietransformation in den Lebensgemeinschaften im Korallenriff zu erfassen, diskutiert.

     

Signaling pathways mediating melanogenesis.

Pigmentation of the skin, due to the synthesis and dispersion of melanin in the epidermis, is of great cosmetic and societal significance. It is also the key physiologic defense against sun-induced injuries such as sunburn, photocarcinogenesis and photoaging. During recent decades, there has been a dramatic increase in skin cancers, including melanoma, due to habitual sun exposure (Rigel, 1992; Weinstock, 1989). At present, in the United States, about one in 75 individuals is projected to develop malignant melanoma during his or her lifetime (Rigel, 1992). Unfortunately, progress in preventing sun-related injuries has been slow, in part due to lack of understanding of the molecular mechanisms involved in pigmentation. This article reviews recent progress in identifying signal transduction pathways that mediate melanogenesis.     

溶血磷脂酸的信号转导途径

溶血磷脂酸（ＬＰＡ）是一种细胞间磷脂信使,它可通过Ｇ蛋白偶联受体引起多种生物学效应,如促进血小板聚集,诱导平滑肌收缩,刺激细胞增殖,抑制细胞分化等。最近研究发现Ｇ蛋白介导的ＬＰＡ信号转导途径至少有四种：（１）刺激磷胆酶Ｃ和磷脂酶Ｄ;（２）抑制腺苷酸环化酶;（３）激活Ｒａｓ及其下游的Ｒａｆ／ＭＡＰＫ途径;（４）Ｒｈｏ信号;粘着斑蛋白的酪氨酸磷酸化和肌动蛋白细胞骨架的重组。这些信号转导途径对细胞的增殖     

Signaling pathways activated by microorganisms

Invasion of viruses and bacteria is initially sensed by the host innate immune system, and evokes a rapid inflammatory response. Nucleotides from RNA viruses are recognized by retinoic-acid-inducible gene I-like helicases and Toll-like receptors, and this recognition triggers signaling cascades that induce antiviral mediators such as type I interferons. By contrast, Toll-like receptors recognizing bacterial components induce the expression of proinflammatory cytokines. Furthermore, recent studies suggest that viral and bacterial DNA also induce interferons in a Toll-independent mechanism, possibly through unidentified cytoplasmic receptor(s).     

Signaling pathways in the epithelial origins of pulmonary fibrosis

Pulmonary fibrosis complicates a number of disease processes and leads to substantial morbidity and mortality. Idiopathic pulmonary fibrosis (IPF) is perhaps the most pernicious and enigmatic form of the greater problem of lung fibrogenesis with a median survival of three years from diagnosis in affected patients. In this review, we will focus on the pathology of IPF as a model of pulmonary fibrotic processes, review possible cellular mechanisms, review current treatment approaches and review two transgenic mouse models of lung fibrosis to provide insight into processes that cause lung fibrosis. We will also summarize the potential utility of signaling pathway inhibitors as a future treatment in pulmonary fibrosis. Finally, we will present data demonstrating a minimal contribution of epithelial-mesenchymal transition in the development of fibrotic lesions in the transforming growth factor-alpha transgenic model of lung fibrosis.     

Signaling pathways from the chloroplast to the nucleus

Genetic and physiological studies have to-date revealed evidence for five signaling pathways by which the chloroplast exerts retrograde control over nuclear genes. One of these pathways is dependent on product(s) of plastid protein synthesis, for another the signal is singlet oxygen, a third employs chloroplast-generated hydrogen peroxide, a fourth is controlled by the redox state of the photosynthetic electron transport chain, and a fifth involves intermediates and possibly proteins of tetrapyrrole biosynthesis. These five pathways may be part of a complex signaling network that links the functional and physiological state of the chloroplast to the nucleus. Mutants defective in various steps of photosynthesis reveal a surprising diversity in nuclear responses suggesting the existence of a complex signaling network.     

Signaling pathways in the epithelial origins of pulmonary fibrosis

Pulmonary fibrosis complicates a number of disease processes and leads to substantial morbidity and mortality. Idiopathic pulmonary fibrosis (IPF) is perhaps the most pernicious and enigmatic form of the greater problem of lung fibrogenesis with a median survival of three years from diagnosis in affected patients. In this review, we will focus on the pathology of IPF as a model of pulmonary fibrotic processes, review possible cellular mechanisms, review current treatment approaches and review two transgenic mouse models of lung fibrosis to provide insight into processes that cause lung fibrosis. We will also summarize the potential utility of signaling pathway inhibitors as a future treatment in pulmonary fibrosis. Finally, we will present data demonstrating a minimal contribution of epithelial-mesenchymal transition in the development of fibrotic lesions in the transforming growth factor-alpha transgenic model of lung fibrosis.Key words: epithelial mesenchymal transition, epidermal growth factor receptor, transforming growth factor alpha