Sponge Behavior and the Chemical Basis of Responses: A Post-Genomic View

2019 ◽  
Vol 59 (4) ◽  
pp. 751-764 ◽  
Author(s):  
Sally P Leys ◽  
Jasmine L Mah ◽  
Paul R McGill ◽  
Laura Hamonic ◽  
Fabio C De Leo ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Atmospheric Pressure ◽  
Water Movement ◽  
Whole Body ◽  
Signal Pathways ◽  
Chemical Signaling ◽  
Electrical Signaling ◽  
Complex Signaling

Abstract Sponges perceive and respond to a range of stimuli. How they do this is still difficult to pin down despite now having transcriptomes and genomes of an array of species. Here we evaluate the current understanding of sponge behavior and present new observations on sponge activity in situ. We also explore biosynthesis pathways available to sponges from data in genomes/transcriptomes of sponges and other non-bilaterians with a focus on exploring the role of chemical signaling pathways mediating sponge behavior and how such chemical signal pathways may have evolved. Sponge larvae respond to light but opsins are not used, nor is there a common photoreceptor molecule or mechanism used across sponge groups. Other cues are gravity and chemicals. In situ recordings of behavior show that both shallow and deep-water sponges move a lot over minutes and hours, and correlation of behavior with temperature, pressure, oxygen, and water movement suggests that at least one sponge responds to changes in atmospheric pressure. The sensors for these cues as far as we know are individual cells and, except in the case of electrical signaling in Hexactinellida, these most likely act as independent effectors, generating a whole-body reaction by the global reach of the stimulus to all parts of the animal. We found no evidence for use of conventional neurotransmitters such as serotonin and dopamine. Intriguingly, some chemicals synthesized by symbiont microbes could mean other more complex signaling occurs, but how that interplay might happen is not understood. Our review suggests chemical signaling pathways found in sponges do not reflect loss of a more complex set.

scholarly journals Role of calcification in aortic degeneration

2020 ◽  
Vol 7 (1) ◽  
pp. 6-21
Author(s):  
D. A. Kostina ◽  
V. E. Uspensky ◽  
D. S. Semenova ◽  
A. S. Kostina ◽  
N. V. Boyarskaya ◽  
...  
Keyword(s):  
Transcription Factors ◽  
Signaling Pathways ◽  
Vascular Calcification ◽  
Vascular Pathology ◽  
Signal Pathways ◽  
Vascular Cells ◽  
Metabolic Dysfunction ◽  
Main Attention ◽  
Biological Regulation

Vascular calcification is a widely-spread pathology with high mortality. It is active bioregulated process that is observed in pathogenesis of different desires, associated with metabolic dysfunction, congenital tissue desires and aging. Signal pathways and transcription factors that are involved in vascular calcification are also takes place in normal osteogenesis and/or vascular development. In the review the main attention is payed to the role of signaling pathways BMP (bone morphogenic protein), Notch, Wnt and to the role of transcription factors BMP2, RUNX2, Msx2 in vascular calcification. Probably, dysfunction of osteogenic signal pathways and transdifferentiation of vascular cells to osteoblast-like cells is a common prosses not only for vascular calcification or mineralization, but is a way of vascular degradation in general. Proosteogenic changes at cellular and molecular level may play role in pathogenesis of a disease without manifestation of vascular mineralization, such as thoracic aortic aneurysm. Ability of vascular cells to change their phenotype to osteophenotype is very likely biologically important ability. Over weakness of calcific signaling pathways activity can also lead to vascular pathology. The aim of the review is to overlook the mechanisms of vascular calcification focusing at the role of signal pathways and vascular cells at this process with particular attention to aortic calcification. Understanding the mechanisms of biological regulation of pro- and antiosteogenic processes in pathology and normal conditions opens new opportunities to influence this prosess in order to correct vascular pathologies.

Cytoarchitecture of the Xenopus thymus following gamma-irradiation

Development ◽  
1987 ◽  
Vol 100 (1) ◽  
pp. 95-105
Author(s):  
JH Russ ◽  
JD Horton
Keyword(s):  
Gamma Irradiation ◽  
Tolerance Induction ◽  
Cell Types ◽  
Whole Body ◽  
Thymic Stromal Cells ◽  
Normal Architecture

This paper describes in vitro and in vivo attempts to deplete the 4- to 8-month-old Xenopus laevis (J strain) thymus of its lymphocyte compartment. Gamma irradiation (2-3000 rad) of the excised thymus, followed by two weeks in organ culture, is effective in removing lymphocytes, but causes drastic reduction in size and loss of normal architecture. In contrast, in vivo whole-body irradiation (3000 rad) and subsequent in situ residence for 8-14 days proves successful in providing a lymphocyte-depleted froglet thymus without loss of cortical and medullary zones. In vivo-irradiated thymuses are about half normal size, lack cortical lymphocytes, but still retain some medullary thymocytes; they show no signs of lymphocyte regeneration when subsequently organ cultured for 2 weeks. Light microscopy of 1 micron, plastic-embedded sections and electron microscopy reveal that a range of thymic stromal cell types are retained and that increased numbers of cysts, mucous and myoid cells are found in the thymus following whole-body irradiation. In vivo-irradiated thymuses are therefore suitable for implantation studies exploring the role of thymic stromal cells in tolerance induction of differentiating T lymphocytes.

Endocannabinoids and Liver Disease. II. Endocannabinoids in the pathogenesis and treatment of liver fibrosis

2008 ◽  
Vol 294 (2) ◽  
pp. G357-G362 ◽  
Author(s):  
Sören V. Siegmund ◽  
Robert F. Schwabe
Keyword(s):  
Liver Fibrosis ◽  
Signaling Pathways ◽  
Hepatic Cirrhosis ◽  
Endocannabinoid System ◽  
Cell Types ◽  
Chronic Injury ◽  
High Incidence ◽  
Complex Signaling ◽  
Injured Liver

Hepatic fibrosis is the response of the liver to chronic injury and is associated with portal hypertension, progression to hepatic cirrhosis, liver failure, and high incidence of hepatocellular carcinoma. On a molecular level, a large number of signaling pathways have been shown to contribute to the activation of fibrogenic cell types and the subsequent accumulation of extracellular matrix in the liver. Recent evidence suggests that the endocannabinoid system is an important part of this complex signaling network. In the injured liver, the endocannabinoid system is upregulated both at the level of endocannabinoids and at the endocannabinoid receptors CB1 and CB2. The hepatic endocannabinoid system mediates both pro- and antifibrogenic effects by activating distinct signaling pathways that differentially affect proliferation and death of fibrogenic cell types. Here we will summarize current findings on the role of the hepatic endocannabinoid system in liver fibrosis and discuss emerging options for its therapeutic exploitation.

scholarly journals Role of the plant heterotrimeric G-proteins in the signal pathways regulation

2019 ◽  
Vol 17 (2) ◽  
pp. 43-54
Author(s):  
Andrey D. Bovin ◽  
Elena A. Dolgikh
Keyword(s):  
Cell Proliferation ◽  
Signaling Pathways ◽  
G Proteins ◽  
Hormonal Regulation ◽  
Abiotic Factors ◽  
Biotic Interactions ◽  
Signal Pathways ◽  
Heterotrimeric G Proteins ◽  
Proliferation Response

Animal and fungal heterotrimeric G-proteins are among the well-known regulators of signaling pathways. Plant studies have shown that G-proteins may also be involved in the regulation of many processes. G-proteins are involved in hormonal regulation, control of cell proliferation, response to abiotic factors, control of biotic interactions and many others. It turned out that with a smaller variety of subunits, G-proteins of plants can have a greater variety of mechanisms for activating and transmitting signals. However, for most processes in plants the mechanisms of operation of heterotrimeric G-proteins remain poorly understood. This review is devoted to the analysis of modern ideas about the structure and functioning of heterotrimeric plant G proteins.

scholarly journals Sam68/KHDRBS1-dependent NF-κB activation confers radioprotection to the colon epithelium in γ-irradiated mice

eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Kai Fu ◽  
Xin Sun ◽  
Eric M Wier ◽  
Andrea Hodgson ◽  
Ryan P Hobbs ◽  
...  
Keyword(s):  
Dna Damage ◽  
Critical Role ◽  
Genotoxic Stress ◽  
Whole Body ◽  
Colon Tissue ◽  
Γ Irradiation ◽  
Apoptotic Genes

Previously we reported that Src-associated-substrate-during-mitosis-of-68kDa (Sam68/KHDRBS1) is pivotal for DNA damage-stimulated NF-κB transactivation of anti-apoptotic genes (Fu et al., 2016). Here we show that Sam68 is critical for genotoxic stress-induced NF-κB activation in the γ-irradiated colon and animal and that Sam68-dependent NF-κB activation provides radioprotection to colon epithelium in vivo. Sam68 deletion diminishes γ-irradiation-triggered PAR synthesis and NF-κB activation in colon epithelial cells (CECs), thus hampering the expression of anti-apoptotic molecules in situ and facilitating CECs to undergo apoptosis in mice post whole-body γ-irradiation (WBIR). Sam68 knockout mice suffer more severe damage in the colon and succumb more rapidly from acute radiotoxicity than the control mice following WBIR. Our results underscore the critical role of Sam68 in orchestrating genotoxic stress-initiated NF-κB activation signaling in the colon tissue and whole animal and reveal the pathophysiological relevance of Sam68-dependent NF-κB activation in colonic cell survival and recovery from extrinsic DNA damage.

scholarly journals The Role of the Signaling Pathways Involved in the Protective Effect of Exogenous Hydrogen Sulfide on Myocardial Ischemia-Reperfusion Injury

2021 ◽  
Vol 9 ◽  
Author(s):  
Shuangyu Lv ◽  
Xiaotian Li ◽  
Shizhen Zhao ◽  
Huiyang Liu ◽  
Honggang Wang
Keyword(s):  
Blood Flow ◽  
Hydrogen Sulfide ◽  
Signaling Pathways ◽  
Structural Changes ◽  
Ischemia Reperfusion Injury ◽  
Tissue Injury ◽  
Ischemia Reperfusion ◽  
Cell Swelling ◽  
Signal Pathways

Ischemia/reperfusion (I/R) injury refers to the functional and structural changes in the process of blood flow recovery after ischemia. In addition to ischemia, the blood flow recovery can also lead to very harmful damage, such as the obvious cell swelling and the irreversible cell necrosis. I/R injury is related with many diseases, including myocardial I/R injury. Myocardial I/R injury refers to the aggravation of ischemic myocardial tissue injury due to sudden disorder of blood circulation. Although there are many studies on myocardial I/R injury, the exact mechanism is not fully understood. Hydrogen sulfide (H2S), like carbon monoxide and nitric oxide, is an important gas signal molecule. It plays an important role in many physiological and pathological processes. Recent studies indicate that H2S can improve myocardial I/R injury, however, its mechanism is not fully understood, especially the involved signal pathways. In this review, we summarize the related researches about the role of the signaling pathways involved in the protective effects of exogenous H2S on myocardial I/R injury, so as to provide theoretical reference for the future in-depth researches.

scholarly journals Insulin Receptor Trafficking: Consequences for Insulin Sensitivity and Diabetes

2019 ◽  
Vol 20 (20) ◽  
pp. 5007 ◽  
Author(s):  
Yang Chen ◽  
Lili Huang ◽  
Xinzhou Qi ◽  
Chen Chen
Keyword(s):  
Insulin Resistance ◽  
Insulin Receptor ◽  
Signaling Pathways ◽  
Severe Insulin Resistance ◽  
Cellular Events ◽  
Wide Range ◽  
Key Factor ◽  
Complex Signaling

Insulin receptor (INSR) has been extensively studied in the area of cell proliferation and energy metabolism. Impaired INSR activities lead to insulin resistance, the key factor in the pathology of metabolic disorders including type 2 diabetes mellitus (T2DM). The mainstream opinion is that insulin resistance begins at a post-receptor level. The role of INSR activities and trafficking in insulin resistance pathogenesis has been largely ignored. Ligand-activated INSR is internalized and trafficked to early endosome (EE), where INSR is dephosphorylated and sorted. INSR can be subsequently conducted to lysosome for degradation or recycled back to the plasma membrane. The metabolic fate of INSR in cellular events implies the profound influence of INSR on insulin signaling pathways. Disruption of INSR-coupled activities has been identified in a wide range of insulin resistance-related diseases such as T2DM. Accumulating evidence suggests that alterations in INSR trafficking may lead to severe insulin resistance. However, there is very little understanding of how altered INSR activities undermine complex signaling pathways to the development of insulin resistance and T2DM. Here, we focus this review on summarizing previous findings on the molecular pathways of INSR trafficking in normal and diseased states. Through this review, we provide insights into the mechanistic role of INSR intracellular processes and activities in the development of insulin resistance and diabetes.

scholarly journals Two swimming modes in Trachymedusae; bell kinematics and the role of giant axons

2021 ◽  
Author(s):  
M. E. Meech ◽  
C. E. Mills ◽  
S. H. D. Haddock ◽  
R. W. Meech
Keyword(s):  
Water Movement ◽  
Swimming Behaviour ◽  
Motor Axons ◽  
Laboratory Measurements ◽  
Video Footage ◽  
Swimming Motion ◽  
Evolutionary Context ◽  
Neural Anatomy

Although members of the Rhopalonematidae family (Cnidaria, Hydrozoa, Trachymedusae) are known to exhibit unusually powerful jet swimming in addition to their more normal slow swimming behaviour, for the most part reports are rare and anecdotal. Many species are found globally at depths of 600 - 2000 m and so observation and collection depends on using remotely operated submersible vehicles. With a combination of in-situ video footage and laboratory measurements, we have quantified kinematic aspects of this dual swimming motion and its electrophysiology. The species included are from two Rhopalonematidae clades; they are Colobonema sericeum, Pantachogon haeckeli, Crossota millsae and two species of Benthocodon. Comparison is made with Aglantha digitale, a species from a third Rhopalonematidae clade brought to the surface by natural water movement. We find that although all Rhopalonematidae appear to have two swimming modes there are marked differences in their neural anatomy, kinematics and physiology. Giant motor axons, known to conduct impulses during fast swimming in A. digitale, are absent from C. sericeum and P. haeckeli. Slow swimming is also different; in C. sericeum and its relatives it is driven by contractions restricted to the base of the bell. These behavioural differences are related to the position of the different clades on a ribosomal DNA-based phylogenetic tree. This finding allows us to pinpoint the phylogenetic branch point leading to the appearance of giant motor axons and escape swimming. They place the remarkable dual swimming behaviour of members of the Rhopalonematidae family into an evolutionary context.

scholarly journals A mitochondrial delicacy: dynamin-related protein 1 and mitochondrial dynamics

2018 ◽  
Vol 315 (1) ◽  
pp. C80-C90 ◽  
Author(s):  
Mason T. Breitzig ◽  
Matthew D. Alleyn ◽  
Richard F. Lockey ◽  
Narasaiah Kolliputi
Keyword(s):  
Signaling Pathways ◽  
Mitochondrial Dynamics ◽  
Mitochondrial Fission ◽  
Pulmonary Diseases ◽  
Related Protein ◽  
Limited Knowledge ◽  
Cellular Bioenergetics ◽  
Complex Signaling ◽  
Mitochondrial Networks

The constant physiological flux of mitochondrial fission and fusion is inextricably tied to the maintenance of cellular bioenergetics and the fluidity of mitochondrial networks. Yet, the intricacies of this dynamic duo remain unclear in diseases that encompass mitochondrial dysregulation. Particularly, the role of the GTPase fission protein dynamin-related protein 1 (Drp1) is of profound interest. Studies have identified that Drp1 participates in complex signaling pathways, suggesting that the function of mitochondria in pathophysiology may extend far beyond energetics alone. Research indicates that, in stressed conditions, Drp1 translocation to the mitochondria leads to elevated fragmentation and mitophagy; however, despite this, there is limited knowledge about the mechanistic regulation of Drp1 in disease conditions. This review highlights literature about fission, fusion, and, more importantly, discusses Drp1 in cardiac, neural, carcinogenic, renal, and pulmonary diseases. The therapeutic desirability for further research into its contribution to diseases that involve mitochondrial dysregulation is also discussed.

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