Cadherin Preserves Cohesion Across Involuting Tissues During C. elegans Neurulation

AbstractThe internalization of the central nervous system, termed neurulation in vertebrates, is a critical step in embryogenesis. Open questions remain as to how force propels coordinated tissue movement during the process, and little is known as to how internalization happens in invertebrates. We show that in C. elegans morphogenesis, apical constriction in the retracting pharynx drives involution of the adjacent neuroectoderm. Localized HMR-1/Cadherin mediates the inter-tissue attachment, as well as within the neuroectoderm to maintain intratissue cohesion. Our results demonstrate that localized HMR-1 is capable of mediating embryo wide reorganization driven by a centrally located force generator, and indicate a non-canonical use of Cadherin on the basal side of an epithelium that may apply to vertebrate neurulation. Additionally, we highlight shared morphology and gene expression in tissues driving involution, which suggests that neuroectoderm involution in C. elegans is potentially homologous with vertebrate neurulation and thus may help elucidate the evolutionary origin of the brain.

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Cadherin preserves cohesion across involuting tissues during C. elegans neurulation

eLife ◽

10.7554/elife.58626 ◽

2020 ◽

Vol 9 ◽

Author(s):

Kristopher M Barnes ◽

Li Fan ◽

Mark W Moyle ◽

Christopher A Brittin ◽

Yichi Xu ◽

...

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Apical Constriction ◽

C Elegans ◽

Open Questions ◽

Tissue Movement ◽

The Central Nervous System ◽

Tissue Attachment ◽

Force Generator ◽

The Brain

The internalization of the central nervous system, termed neurulation in vertebrates, is a critical step in embryogenesis. Open questions remain regarding how force propels coordinated tissue movement during the process, and little is known as to how internalization happens in invertebrates. We show that in C. elegans morphogenesis, apical constriction in the retracting pharynx drives involution of the adjacent neuroectoderm. HMR-1/cadherin mediates this process via inter-tissue attachment, as well as cohesion within the neuroectoderm. Our results demonstrate that HMR-1 is capable of mediating embryo-wide reorganization driven by a centrally located force generator, and indicate a non-canonical use of cadherin on the basal side of an epithelium that may apply to vertebrate neurulation. Additionally, we highlight shared morphology and gene expression in tissues driving involution, which suggests that neuroectoderm involution in C. elegans is potentially homologous with vertebrate neurulation and thus may help elucidate the evolutionary origin of the brain.

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From Genes to Behavior in the Vestibular System

Otolaryngology ◽

10.1016/s0194-5998(98)70061-0 ◽

1998 ◽

Vol 119 (3) ◽

pp. 263-275 ◽

Cited By ~ 25

Author(s):

Robert Baker

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Behavioral Correlates ◽

Reticulospinal Neurons ◽

Molecular Approaches ◽

Signaling Mechanisms ◽

The Central Nervous System ◽

Vertebrate Embryos ◽

Motor Nuclei ◽

The Brain

The central nervous system of all vertebrate embryos is derived from a series of conspicuous segments, called neuromeres, that are particularly visible in the midbrain and hindbrain areas, giving rise to the brain stem sensory and motor nuclei. This article focuses on a series of eight embryonic rhombomeric segments whose progeny can be identified in adults by the locations of iteratively homologous reticulospinal neurons and cranial motor nuclei IV through XII. Evidence shows that these rhombomeric units represent domains of gene expression, lineage restriction, and accordingly, individual vestibular neuronal phenotypes with unique oculomotor and spinal projections. Preliminary electrophysiologic and behavioral correlates of a few vestibulo-oculomotor subgroups are used as examples to illustrate the hypothesis that homologous vestibular phenotypes likely exist in all taxa because the genetic prepattern is already well established in primitive vertebrates. Finally, the segmented hindbrain arrangement responsible for the longitudinally arranged column of vestibular subnuclei is placed in perspective with genetic and molecular approaches that will eventually permit a causal reconstruction of the signaling mechanisms responsible for the development of unique vestibular subgroups.

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Differential Regulation of Interferon Regulatory Factor (IRF)-7 and IRF-9 Gene Expression in the Central Nervous System during Viral Infection

Journal of Virology ◽

10.1128/jvi.79.12.7514-7527.2005 ◽

2005 ◽

Vol 79 (12) ◽

pp. 7514-7527 ◽

Cited By ~ 49

Author(s):

Shalina S. Ousman ◽

Jianping Wang ◽

Iain L. Campbell

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Nervous System ◽

Viral Infection ◽

Mononuclear Cells ◽

Lymphocytic Choriomeningitis ◽

The Central Nervous System ◽

Ifn Γ ◽

The Brain ◽

Lcmv Infection

ABSTRACT Interferon regulatory factors (IRFs) are a family of transcription factors involved in the regulation of the interferons (IFNs) and other genes that may have an essential role in antiviral defense in the central nervous system, although this is currently not well defined. Therefore, we examined the regulation of IRF gene expression in the brain during viral infection. Several IRF genes (IRF-2, -3, -5, -7, and -9) were expressed at low levels in the brain of uninfected mice. Following intracranial infection with lymphocytic choriomeningitis virus (LCMV), expression of the IRF-7 and IRF-9 genes increased significantly by day 2. IRF-7 and IRF-9 gene expression in the brain was widespread at sites of LCMV infection, with the highest levels in infiltrating mononuclear cells, microglia/macrophages, and neurons. IRF-7 and IRF-9 gene expression was increased in LCMV-infected brain from IFN-γ knockout (KO) but not IFN-α/βR KO animals. In the brain, spleen, and liver or cultured glial and spleen cells, IRF-7 but not IRF-9 gene expression increased with delayed kinetics in the absence of STAT1 but not STAT2 following LCMV infection or IFN-α treatment, respectively. The stimulation of IRF-7 gene expression by IFN-α in glial cell culture was prevented by cycloheximide. Thus, (i) many of the IRF genes were expressed constitutively in the mouse brain; (ii) the IRF-7 and IRF-9 genes were upregulated during viral infection, a process dependent on IFN-α/β but not IFN-γ; and (iii) IRF-7 but not IRF-9 gene expression can be stimulated in a STAT1-independent but STAT2-dependent fashion via unidentified indirect pathways coupled to the activation of the IFN-α/β receptor.

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Glucuronyl 3-sulfate occurs exclusively on distal unmyelinated terminals of selected sensory neurons in the peripheral nervous system

Proceedings, annual meeting, Electron Microscopy Society of America ◽

10.1017/s0424820100141160 ◽

1995 ◽

Vol 53 ◽

pp. 958-959

Author(s):

S.S. Spicer ◽

B.A. Schulte

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Cerebral Cortex ◽

Peripheral Nervous System ◽

Sensory Neurons ◽

Sensory Nerves ◽

Tissue Antigens ◽

The Central Nervous System ◽

The Brain ◽

Leu 7

Generation of monoclonal antibodies (MAbs) against tissue antigens has yielded several (VC1.1, HNK- 1, L2, 4F4 and anti-leu 7) which recognize the unique sugar epitope, glucuronyl 3-sulfate (Glc A3- SO4). In the central nervous system, these MAbs have demonstrated Glc A3-SO4 at the surface of neurons in the cerebral cortex, the cerebellum, the retina and other widespread regions of the brain.Here we describe the distribution of Glc A3-SO4 in the peripheral nervous system as determined by immunostaining with a MAb (VC 1.1) developed against antigen in the cat visual cortex. Outside the central nervous system, immunoreactivity was observed only in peripheral terminals of selected sensory nerves conducting transduction signals for touch, hearing, balance and taste. On the glassy membrane of the sinus hair in murine nasal skin, just deep to the ringwurt, VC 1.1 delineated an intensely stained, plaque-like area (Fig. 1). This previously unrecognized structure of the nasal vibrissae presumably serves as a tactile end organ and to our knowledge is not demonstrable by means other than its selective immunopositivity with VC1.1 and its appearance as a densely fibrillar area in H&E stained sections.

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Central Nerve System Impairment, AMA Guides, Sixth Edition: An Overview

Guides Newsletter ◽

10.1001/amaguidesnewsletters.2018.janfeb03 ◽

2018 ◽

Vol 23 (1) ◽

pp. 10-13

Author(s):

James B. Talmage ◽

Jay Blaisdell

Keyword(s):

Spinal Cord ◽

Central Nervous System ◽

Nervous System ◽

Neurological Impairment ◽

Sixth Edition ◽

Central Nerve System ◽

The Central Nervous System ◽

The One ◽

Nerve System ◽

The Brain

Abstract Injuries that affect the central nervous system (CNS) can be catastrophic because they involve the brain or spinal cord, and determining the underlying clinical cause of impairment is essential in using the AMA Guides to the Evaluation of Permanent Impairment (AMA Guides), in part because the AMA Guides addresses neurological impairment in several chapters. Unlike the musculoskeletal chapters, Chapter 13, The Central and Peripheral Nervous System, does not use grades, grade modifiers, and a net adjustment formula; rather the chapter uses an approach that is similar to that in prior editions of the AMA Guides. The following steps can be used to perform a CNS rating: 1) evaluate all four major categories of cerebral impairment, and choose the one that is most severe; 2) rate the single most severe cerebral impairment of the four major categories; 3) rate all other impairments that are due to neurogenic problems; and 4) combine the rating of the single most severe category of cerebral impairment with the ratings of all other impairments. Because some neurological dysfunctions are rated elsewhere in the AMA Guides, Sixth Edition, the evaluator may consult Table 13-1 to verify the appropriate chapter to use.

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Gene Expression in The Central Nervous System

10.1016/s0079-6123(08)x6097-2 ◽

1995 ◽

Keyword(s):

Gene Expression ◽

Central Nervous System ◽

Nervous System ◽

The Central Nervous System

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Faculty Opinions recommendation of The brain as an immune privileged site: dendritic cells of the central nervous system inhibit T cell activation.

Faculty Opinions – Post-Publication Peer Review of the Biomedical Literature ◽

10.3410/f.1014090.200835 ◽

2003 ◽

Author(s):

Magdalena Plebanski

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Dendritic Cells ◽

T Cell ◽

T Cell Activation ◽

Cell Activation ◽

The Central Nervous System ◽

The Brain ◽

Privileged Site

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RAS in the Central Nervous System: Potential Role in Neuropsychiatric Disorders

Current Medicinal Chemistry ◽

10.2174/0929867325666180226102358 ◽

2018 ◽

Vol 25 (28) ◽

pp. 3333-3352 ◽

Cited By ~ 21

Author(s):

Natalia Pessoa Rocha ◽

Ana Cristina Simoes e Silva ◽

Thiago Ruiz Rodrigues Prestes ◽

Victor Feracin ◽

Caroline Amaral Machado ◽

...

Keyword(s):

Blood Pressure ◽

Central Nervous System ◽

Nervous System ◽

Therapeutic Potential ◽

Neuropsychiatric Disorders ◽

Extensive Literature ◽

Ang Ii ◽

Mas Receptor ◽

The Central Nervous System ◽

The Brain

Background: The Renin-Angiotensin System (RAS) is a key regulator of cardiovascular and renal homeostasis, but also plays important roles in mediating physiological functions in the central nervous system (CNS). The effects of the RAS were classically described as mediated by angiotensin (Ang) II via angiotensin type 1 (AT1) receptors. However, another arm of the RAS formed by the angiotensin converting enzyme 2 (ACE2), Ang-(1-7) and the Mas receptor has been a matter of investigation due to its important physiological roles, usually counterbalancing the classical effects exerted by Ang II. Objective: We aim to provide an overview of effects elicited by the RAS, especially Ang-(1-7), in the brain. We also aim to discuss the therapeutic potential for neuropsychiatric disorders for the modulation of RAS. Method: We carried out an extensive literature search in PubMed central. Results: Within the brain, Ang-(1-7) contributes to the regulation of blood pressure by acting at regions that control cardiovascular functions. In contrast with Ang II, Ang-(1-7) improves baroreflex sensitivity and plays an inhibitory role in hypothalamic noradrenergic neurotransmission. Ang-(1-7) not only exerts effects related to blood pressure regulation, but also acts as a neuroprotective component of the RAS, for instance, by reducing cerebral infarct size, inflammation, oxidative stress and neuronal apoptosis. Conclusion: Pre-clinical evidence supports a relevant role for ACE2/Ang-(1-7)/Mas receptor axis in several neuropsychiatric conditions, including stress-related and mood disorders, cerebrovascular ischemic and hemorrhagic lesions and neurodegenerative diseases. However, very few data are available regarding the ACE2/Ang-(1-7)/Mas receptor axis in human CNS.

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Ethanolamine: A Potential Promoiety with Additional Effects in the Brain

CNS & Neurological Disorders - Drug Targets ◽

10.2174/1871527319999201211204645 ◽

2020 ◽

Vol 19 ◽

Author(s):

Asfree Gwanyanya ◽

Christie Nicole Godsmark ◽

Roisin Kelly-Laubscher

Keyword(s):

Central Nervous System ◽

Nervous System ◽

Drug Design ◽

Cell Signaling ◽

Blood Brain Barrier ◽

Brain Barrier ◽

The Central Nervous System ◽

Bioactive Molecule ◽

Positive Functions ◽

The Brain

Abstract: Ethanolamine is a bioactive molecule found in several cells, including those in the central nervous system (CNS). In the brain, ethanolamine and ethanolamine-related molecules have emerged as prodrug moieties that can promote drug movement across the blood-brain barrier. This improvement in the ability to target drugs to the brain may also mean that in the process ethanolamine concentrations in the brain are increased enough for ethanolamine to exert its own neurological ac-tions. Ethanolamine and its associated products have various positive functions ranging from cell signaling to molecular storage, and alterations in their levels have been linked to neurodegenerative conditions such as Alzheimer’s disease. This mini-review focuses on the effects of ethanolamine in the CNS and highlights the possible implications of these effects for drug design.

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