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Results: 1 to 10 of 43

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Neuronal Fat and Dendrite Morphogenesis: The Goldilocks Effect.
Sundararajan L, Miller DM
(2018) Trends Neurosci 41: 250-252
MeSH Terms: Animals, Dendrites, Drosophila, Drosophila Proteins, Larva, Morphogenesis, Neurogenesis
Show Abstract · Added March 26, 2019
Two recent studies by Meltzer et al. and Ziegler et al. use Drosophila larvae to demonstrate that cell-autonomous regulation of lipid biosynthesis defines the complexity and function of highly branched nociceptive neurons. Their findings show that lipid biosynthesis in the neuron is fine-tuned for optimal dendrite morphology and sensitivity.
Copyright © 2018 Elsevier Ltd. All rights reserved.
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MeSH Terms
Defining the interaction of the protease CpaA with its type II secretion chaperone CpaB and its contribution to virulence in species.
Kinsella RL, Lopez J, Palmer LD, Salinas ND, Skaar EP, Tolia NH, Feldman MF
(2017) J Biol Chem 292: 19628-19638
MeSH Terms: Acinetobacter, Animals, Factor V, Larva, Mice, Mice, Inbred C57BL, Molecular Chaperones, Peptide Hydrolases, Protein Binding, Proteolysis, Spleen, Virulence
Show Abstract · Added March 15, 2018
, , and are a frequent cause of multidrug-resistant, healthcare-associated infections. Our previous work demonstrated that M2 possesses a functional type II secretion system (T2SS) that is required for full virulence. Further, we identified the metallo-endopeptidase CpaA, which has been shown previously to cleave human Factor V and deregulate blood coagulation, as the most abundant type II secreted effector protein. We also demonstrated that its secretion is dependent on CpaB, a membrane-bound chaperone. In this study, we show that CpaA expression and secretion are conserved across several medically relevant species. Additionally, we demonstrate that deletion of results in attenuation of M2 virulence in moth and mouse models. The virulence defects resulting from the deletion of were comparable with those observed upon abrogation of T2SS activity. The virulence defects resulting from the deletion of are comparable with those observed upon abrogation of T2SS activity. We also show that CpaA and CpaB strongly interact, forming a complex in a 1:1 ratio. Interestingly, deletion of the N-terminal transmembrane domain of CpaB results in robust secretion of CpaA and CpaB, indicating that the transmembrane domain is dispensable for CpaA secretion and likely functions to retain CpaB inside the cell. Limited proteolysis of spheroplasts revealed that the C-terminal domain of CpaB is exposed to the periplasm, suggesting that this is the site where CpaA and CpaB interact Last, we show that CpaB does not abolish the proteolytic activity of CpaA against human Factor V. We conclude that CpaA is, to the best of our knowledge, the first characterized, virulence factor secreted by species.
© 2017 by The American Society for Biochemistry and Molecular Biology, Inc.
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12 MeSH Terms
A transcription factor network controls cell migration and fate decisions in the developing zebrafish pineal complex.
Khuansuwan S, Clanton JA, Dean BJ, Patton JG, Gamse JT
(2016) Development 143: 2641-50
MeSH Terms: Animals, Body Patterning, Cell Count, Cell Lineage, Cell Movement, Gene Dosage, Gene Expression Regulation, Developmental, Gene Regulatory Networks, Habenula, Larva, Mosaicism, Mutation, Neurons, Pineal Gland, Retinal Rod Photoreceptor Cells, Transcription Factors, Zebrafish, Zebrafish Proteins
Show Abstract · Added August 4, 2017
The zebrafish pineal complex consists of four cell types (rod and cone photoreceptors, projection neurons and parapineal neurons) that are derived from a single pineal complex anlage. After specification, parapineal neurons migrate unilaterally away from the rest of the pineal complex whereas rods, cones and projection neurons are non-migratory. The transcription factor Tbx2b is important for both the correct number and migration of parapineal neurons. We find that two additional transcription factors, Flh and Nr2e3, negatively regulate parapineal formation. Flh induces non-migratory neuron fates and limits the extent of parapineal specification, in part by activation of Nr2e3 expression. Tbx2b is positively regulated by Flh, but opposes Flh action during specification of parapineal neurons. Loss of parapineal neuron specification in Tbx2b-deficient embryos can be partially rescued by loss of Nr2e3 or Flh function; however, parapineal migration absolutely requires Tbx2b activity. We conclude that cell specification and migration in the pineal complex are regulated by a network of at least three transcription factors.
© 2016. Published by The Company of Biologists Ltd.
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18 MeSH Terms
Epidermis-Derived Semaphorin Promotes Dendrite Self-Avoidance by Regulating Dendrite-Substrate Adhesion in Drosophila Sensory Neurons.
Meltzer S, Yadav S, Lee J, Soba P, Younger SH, Jin P, Zhang W, Parrish J, Jan LY, Jan YN
(2016) Neuron 89: 741-55
MeSH Terms: Animals, Animals, Genetically Modified, Cell Communication, Dendrites, Drosophila, Drosophila Proteins, Epidermis, Focal Adhesion Kinase 1, Gene Expression Regulation, Developmental, Green Fluorescent Proteins, Immunoprecipitation, Larva, Mechanistic Target of Rapamycin Complex 2, Molecular Biology, Multiprotein Complexes, Mutation, Nerve Tissue Proteins, Receptors, Cell Surface, Semaphorins, Sensory Receptor Cells, TOR Serine-Threonine Kinases, Transfection
Show Abstract · Added February 9, 2016
Precise patterning of dendritic arbors is critical for the wiring and function of neural circuits. Dendrite-extracellular matrix (ECM) adhesion ensures that the dendrites of Drosophila dendritic arborization (da) sensory neurons are properly restricted in a 2D space, and thereby facilitates contact-mediated dendritic self-avoidance and tiling. However, the mechanisms regulating dendrite-ECM adhesion in vivo are poorly understood. Here, we show that mutations in the semaphorin ligand sema-2b lead to a dramatic increase in self-crossing of dendrites due to defects in dendrite-ECM adhesion, resulting in a failure to confine dendrites to a 2D plane. Furthermore, we find that Sema-2b is secreted from the epidermis and signals through the Plexin B receptor in neighboring neurons. Importantly, we find that Sema-2b/PlexB genetically and physically interacts with TORC2 complex, Tricornered (Trc) kinase, and integrins. These results reveal a novel role for semaphorins in dendrite patterning and illustrate how epidermal-derived cues regulate neural circuit assembly.
Copyright © 2016 Elsevier Inc. All rights reserved.
1 Communities
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22 MeSH Terms
Circadian modulation of dopamine levels and dopaminergic neuron development contributes to attention deficiency and hyperactive behavior.
Huang J, Zhong Z, Wang M, Chen X, Tan Y, Zhang S, He W, He X, Huang G, Lu H, Wu P, Che Y, Yan YL, Postlethwait JH, Chen W, Wang H
(2015) J Neurosci 35: 2572-87
MeSH Terms: Animals, Animals, Genetically Modified, Attention Deficit Disorder with Hyperactivity, Avoidance Learning, Behavior, Animal, Circadian Rhythm, Dopamine, Dopaminergic Neurons, Impulsive Behavior, Larva, Mice, Motor Activity, NIH 3T3 Cells, Period Circadian Proteins, Tyrosine 3-Monooxygenase, Zebrafish, Zebrafish Proteins
Show Abstract · Added February 20, 2015
Attention-deficit/hyperactivity disorder (ADHD) is one of the most prevalent psychiatric disorders in children and adults. While ADHD patients often display circadian abnormalities, the underlying mechanisms are unclear. Here we found that the zebrafish mutant for the circadian gene period1b (per1b) displays hyperactive, impulsive-like, and attention deficit-like behaviors and low levels of dopamine, reminiscent of human ADHD patients. We found that the circadian clock directly regulates dopamine-related genes monoamine oxidase and dopamine β hydroxylase, and acts via genes important for the development or maintenance of dopaminergic neurons to regulate their number and organization in the ventral diencephalic posterior tuberculum. We then found that Per1 knock-out mice also display ADHD-like symptoms and reduced levels of dopamine, thereby showing highly conserved roles of the circadian clock in ADHD. Our studies demonstrate that disruption of a circadian clock gene elicits ADHD-like syndrome. The circadian model for attention deficiency and hyperactive behavior sheds light on ADHD pathogenesis and opens avenues for exploring novel targets for diagnosis and therapy for this common psychiatric disorder.
Copyright © 2015 the authors 0270-6474/15/352572-16$15.00/0.
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17 MeSH Terms
Comparative structural and functional analysis of the larval and adult dorsal vessel and its role in hemolymph circulation in the mosquito Anopheles gambiae.
League GP, Onuh OC, Hillyer JF
(2015) J Exp Biol 218: 370-80
MeSH Terms: Animals, Anopheles, Female, Heart, Hemolymph, Larva, Metamorphosis, Biological, Muscle Contraction, Video Recording
Show Abstract · Added February 5, 2016
Hemolymph circulation in insects is driven primarily by the contractile action of a dorsal vessel, which is divided into an abdominal heart and a thoracic aorta. As holometabolous insects, mosquitoes undergo striking morphological and physiological changes during metamorphosis. This study presents a comprehensive structural and functional analysis of the larval and adult dorsal vessel in the malaria mosquito Anopheles gambiae. Using intravital video imaging we show that, unlike the adult heart, the larval heart contracts exclusively in the anterograde direction and does not undergo heartbeat directional reversals. The larval heart contracts 24% slower than the adult heart, and hemolymph travels across the larval dorsal vessel at a velocity that is 68% slower than what is seen in adults. By fluorescently labeling muscle tissue we show that although the general structure of the heart and its ostia are similar across life stages, the heart-associated alary muscles are significantly less robust in larvae. Furthermore, unlike the adult ostia, which are the entry points for hemolymph into the heart, the larval ostia are almost entirely lacking in incurrent function. Instead, hemolymph enters the larval heart through incurrent openings located at the posterior terminus of the heart. These posterior openings are structurally similar across life stages, but in adults have an opposite, excurrent function. Finally, the larval aorta and heart differ significantly in the arrangement of their cardiomyocytes. In summary, this study provides an in-depth developmental comparison of the circulatory system of larval and adult mosquitoes.
© 2015. Published by The Company of Biologists Ltd.
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1 Members
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9 MeSH Terms
Thermolysin damages animal life through degradation of plasma proteins enhanced by rapid cleavage of serpins and activation of proteases.
Kong L, Lu A, Guan J, Yang B, Li M, Hillyer JF, Ramarao N, Söderhäll K, Liu C, Ling E
(2015) Arch Insect Biochem Physiol 88: 64-84
MeSH Terms: Animals, Blood Proteins, Bombyx, Catechol Oxidase, Drosophila melanogaster, Enzyme Precursors, Hemolymph, Insect Proteins, Larva, Melanins, Peptide Hydrolases, Serine Endopeptidases, Serine Proteases, Serpins, Thermolysin, Virulence Factors
Show Abstract · Added February 5, 2016
Thermolysin, a metallopeptidase secreted by pathogenic microbes, is concluded as an important virulence factor due to cleaving purified host proteins in vitro. Using the silkworm Bombyx mori as a model system, we found that thermolysin injection into larvae induces the destruction of the coagulation response and the activation of hemolymph melanization, which results in larval death. Thermolysin triggers the rapid degradation of insect and mammalian plasma proteins at a level that is considerably greater than expected in vitro and/or in vivo. To more specifically explore the mechanism, thermolysin-induced changes to key proteins belonging to the insect melanization pathway were assessed as a window for observing plasma protein cleavage. The application of thermolysin induced the rapid cleavage of the melanization negative regulator serpin-3, but did not directly activate the melanization rate-limiting enzyme prophenoloxidase (PPO) or the terminal serine proteases responsible for PPO activation. Terminal serine proteases of melanization are activated indirectly after thermolysin exposure. We hypothesize that thermolysin induces the rapid degradation of serpins and the activation of proteases directly or indirectly, boosting uncontrolled plasma protein degradation in insects and mammalians.
© 2014 Wiley Periodicals, Inc.
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16 MeSH Terms
Bromine is an essential trace element for assembly of collagen IV scaffolds in tissue development and architecture.
McCall AS, Cummings CF, Bhave G, Vanacore R, Page-McCaw A, Hudson BG
(2014) Cell 157: 1380-92
MeSH Terms: Animals, Basement Membrane, Bromine, Cell Line, Collagen, Drosophila, Extracellular Matrix Proteins, Humans, Imines, Larva, Mice, Peroxidase, Trace Elements
Show Abstract · Added June 10, 2014
Bromine is ubiquitously present in animals as ionic bromide (Br(-)) yet has no known essential function. Herein, we demonstrate that Br(-) is a required cofactor for peroxidasin-catalyzed formation of sulfilimine crosslinks, a posttranslational modification essential for tissue development and architecture found within the collagen IV scaffold of basement membranes (BMs). Bromide, converted to hypobromous acid, forms a bromosulfonium-ion intermediate that energetically selects for sulfilimine formation. Dietary Br deficiency is lethal in Drosophila, whereas Br replenishment restores viability, demonstrating its physiologic requirement. Importantly, Br-deficient flies phenocopy the developmental and BM defects observed in peroxidasin mutants and indicate a functional connection between Br(-), collagen IV, and peroxidasin. We establish that Br(-) is required for sulfilimine formation within collagen IV, an event critical for BM assembly and tissue development. Thus, bromine is an essential trace element for all animals, and its deficiency may be relevant to BM alterations observed in nutritional and smoking-related disease. PAPERFLICK:
Copyright © 2014 Elsevier Inc. All rights reserved.
1 Communities
4 Members
1 Resources
13 MeSH Terms
Myotropic effects of FMRFamide containing peptides on the heart of the mosquito Anopheles gambiae.
Hillyer JF, Estévez-Lao TY, de la Parte LE
(2014) Gen Comp Endocrinol 202: 15-25
MeSH Terms: Amino Acid Sequence, Animals, Anopheles, FMRFamide, Female, Gene Expression Regulation, Developmental, Genes, Insect, Heart, Larva, Molecular Sequence Data, Myocardial Contraction, Receptors, Invertebrate Peptide, Time Factors
Show Abstract · Added February 5, 2016
FMRFamide-like peptides (FLPs) are produced by invertebrate and vertebrate animals, and regulate diverse physiological processes. In insects, several FLPs modulate heart physiology, with some increasing and others decreasing dorsal vessel contraction dynamics. Here, we describe the FMRFamide gene structure in the mosquito, Anopheles gambiae, quantify the developmental and spatial expression of FMRFamide and its putative receptor (FMRFamideR), and show that the peptides FMRFamide and SALDKNFMRFamide have complex myotropic properties. RACE sequencing showed that the FMRFamide gene encodes eight putative FLPs and is alternatively spliced. Of the eight FLPs, only one is shared by A. gambiae, Aedes aegypti and Culex quinquefasciatus: SALDKNFMRFamide. Quantitative PCR showed that peak expression of FMRFamide and FMRFamideR occurs in second instar larvae and around eclosion. In adults, FMRFamide is primarily transcribed in the head and thorax, and FMRFamideR is primarily transcribed in the thorax. Intravital video imaging of mosquitoes injected FMRFamide and SALDKNFMRFamide revealed that at low doses these peptides increase heart contraction rates. At high doses, however, these peptides decrease heart contraction rates and alter the proportional directionality of heart contractions. Taken altogether, these data describe the FMRFamide gene in A. gambiae, and show that FLPs are complex modulators of mosquito circulatory physiology.
Copyright © 2014 Elsevier Inc. All rights reserved.
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13 MeSH Terms
Overnutrition induces β-cell differentiation through prolonged activation of β-cells in zebrafish larvae.
Li M, Maddison LA, Page-McCaw P, Chen W
(2014) Am J Physiol Endocrinol Metab 306: E799-807
MeSH Terms: Animals, Animals, Genetically Modified, Calcium Channels, L-Type, Cell Count, Cell Differentiation, Disease Models, Animal, Embryo, Nonmammalian, Glucokinase, Insulin-Secreting Cells, KATP Channels, Larva, Membrane Potentials, Overnutrition, Potassium Channels, Inwardly Rectifying, Zebrafish
Show Abstract · Added April 24, 2014
Insulin from islet β-cells maintains glucose homeostasis by stimulating peripheral tissues to remove glucose from circulation. Persistent elevation of insulin demand increases β-cell number through self-replication or differentiation (neogenesis) as part of a compensatory response. However, it is not well understood how a persistent increase in insulin demand is detected. We have previously demonstrated that a persistent increase in insulin demand by overnutrition induces compensatory β-cell differentiation in zebrafish. Here, we use a series of pharmacological and genetic analyses to show that prolonged stimulation of existing β-cells is necessary and sufficient for this compensatory response. In the absence of feeding, tonic, but not intermittent, pharmacological activation of β-cell secretion was sufficient to induce β-cell differentiation. Conversely, drugs that block β-cell secretion, including an ATP-sensitive potassium (K ATP) channel agonist and an L-type Ca(2+) channel blocker, suppressed overnutrition-induced β-cell differentiation. Genetic experiments specifically targeting β-cells confirm existing β-cells as the overnutrition sensor. First, inducible expression of a constitutively active K ATP channel in β-cells suppressed the overnutrition effect. Second, inducible expression of a dominant-negative K ATP mutant induced β-cell differentiation independent of nutrients. Third, sensitizing β-cell metabolism by transgenic expression of a hyperactive glucokinase potentiated differentiation. Finally, ablation of the existing β-cells abolished the differentiation response. Taken together, these data establish that overnutrition induces β-cell differentiation in larval zebrafish through prolonged activation of β-cells. These findings demonstrate an essential role for existing β-cells in sensing overnutrition and compensating for their own insufficiency by recruiting additional β-cells.
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15 MeSH Terms