The formation of commissures in the Drosophila CNS depends on the midline cells and on the Notch gene

Development ◽  
1994 ◽  
Vol 120 (1) ◽  
pp. 123-133 ◽  
Author(s):  
T.V. Menne ◽  
C. Klambt
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Germ Line ◽  
Temperature Shift ◽  
Close Relation ◽  
Notch Gene ◽  
Cns Midline ◽  
Midline Cells ◽  
Blastoderm Stage ◽  
Commissural Connections

The commissures of the Drosophila central nervous system (CNS) are formed in close relation to the ventral midline cells, a morphologically distinct set of cells located at the midline of the developing CNS. To analyze the function of these cells during commissure formation, we looked for mutations that result in the absence of commissures. One example of a gene that can give rise to such a phenotype is the neurogenic gene Notch. Here we show that mutant Notch embryos are devoid of commissural connections and have an abnormal midline. The midline cells of the embryonic Drosophila CNS are specified during the blastoderm stage about two hours before the first neuroblasts start to delaminate from the neurogenic region. To analyze Notch function for commissure development further, we took advantage of the Notchts1 allele. Temperature-shift experiments demonstrated that the lack of commissures in mutant Notch embryos results from defects in the analage of the CNS midline cells. Here maternal as well as zygotic Notch function are required for the correct activation of the gene single-minded, since mutant Notch embryos derived from germ-line clones lack most of the single-minded-positive midline cells.

scholarly journals Control of CNS midline transcription by asymmetric E-box-like elements: similarity to xenobiotic responsive regulation

Development ◽  
1994 ◽  
Vol 120 (12) ◽  
pp. 3563-3569 ◽  
Author(s):  
K.A. Wharton ◽  
R.G. Franks ◽  
Y. Kasai ◽  
S.T. Crews
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Germ Line ◽  
Embryonic Cells ◽  
Helix Loop Helix ◽  
E Box ◽  
Cns Midline ◽  
Midline Cells ◽  
Separate Identity ◽  
Xenobiotic Response

Central nervous system midline cells constitute a discrete group of Drosophila embryonic cells with numerous functional and developmental roles. Corresponding to their separate identity, the midline cells display patterns of gene expression distinct from the lateral central nervous system. A conserved 5 base pair sequence (ACGTG) was identified in central nervous system midline transcriptional enhancers of three genes. Germ-line transformation experiments indicate that this motif forms the core of an element required for central nervous system midline transcription. The central nervous system midline element is related to the mammalian xenobiotic response element, which regulates transcription of genes that metabolize aromatic hydrocarbons. These data suggest a model whereby related basic-helix-loop-helix-PAS proteins interact with asymmetric E-box-like target sequences to control these disparate processes.

scholarly journals Commissureless is required both in commissural neurones and midline cells for axon guidance across the midline

Development ◽  
2002 ◽  
Vol 129 (12) ◽  
pp. 2947-2956 ◽  
Author(s):  
Marios Georgiou ◽  
Guy Tear
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Rna Interference ◽  
Protein Expression ◽  
Axon Guidance ◽  
Contralateral Side ◽  
Commissural Axons ◽  
Midline Crossing ◽  
The Central Nervous System ◽  
Midline Cells

In the absence of Commissureless (Comm) function, axons are unable to extend across the central nervous system midline. Comm downregulates levels of Roundabout (Robo), a receptor for the midline repellent Slit, in order to allow axons to cross the midline. comm transcript is expressed at high levels in the midline glia and Comm protein accumulates on axons at the midline. This has led to the hypothesis that Comm moves from the midline glia to the axons, where it can reduce Robo levels. We have found that expression of Comm in the midline cells is unable to rescue the comm phenotype and that tagged versions of Comm are not transferred to axons. A re-examination of Comm protein expression and the use of targeted RNA interference reveal that correct midline crossing requires that Comm is expressed in the commissural axons and midline glia. We suggest that accumulation of Comm protein at the midline spatially limits Comm activity and prevents it from being active on the contralateral side of the central nervous system.

scholarly journals Innate Immunity and Neuroinflammation

2013 ◽  
Vol 2013 ◽  
pp. 1-19 ◽  
Author(s):  
Abhishek Shastri ◽  
Domenico Marco Bonifati ◽  
Uday Kishore
Keyword(s):  
Central Nervous System ◽  
Pattern Recognition ◽  
Innate Immunity ◽  
Nervous System ◽  
Immune System ◽  
Innate Immune System ◽  
Close Relation ◽  
Innate Immune ◽  
Beneficial Effects ◽  
Chronic Neuroinflammation

Inflammation of central nervous system (CNS) is usually associated with trauma and infection. Neuroinflammation occurs in close relation to trauma, infection, and neurodegenerative diseases. Low-level neuroinflammation is considered to have beneficial effects whereas chronic neuroinflammation can be harmful. Innate immune system consisting of pattern-recognition receptors, macrophages, and complement system plays a key role in CNS homeostasis following injury and infection. Here, we discuss how innate immune components can also contribute to neuroinflammation and neurodegeneration.

CNS midline cells influence the division and survival of lateral glia in theDrosophila nervous system

genesis ◽  
2007 ◽  
Vol 45 (5) ◽  
pp. 266-274 ◽  
Author(s):  
So Hee Kim ◽  
Hyeon Ju Kim ◽  
Soo Youn Kim ◽  
Sang-Hak Jeon ◽  
Sang Hee Kim
Keyword(s):  
Nervous System ◽  
Cns Midline ◽  
Midline Cells

scholarly journals Diffuse Midline Glioma, H3K27M-mutant Subtype, Confused for Viral Encephalitis: A Case Report

2020 ◽  
pp. 1-4
Author(s):  
Weidong Yang ◽  
Cong Fu ◽  
Yiyao Cao ◽  
Zhijuan Chen ◽  
Qing Yu ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Viral Encephalitis ◽  
Clinical Symptoms ◽  
Early Recognition ◽  
Clinical Manifestations ◽  
Young Male ◽  
Contrast Enhanced Ct ◽  
Cns Midline ◽  
Diffuse Midline Glioma

The diffuse midline glioma, H3K27M-mutant subtype, occurs mainly in children as a result of mutations in the histone H3 (H3F3A) and HIST1H3B (K27M) genes and is characterized by diffuse tumor growth in central nervous system (CNS) midline structures. Due to its nonspecific clinical manifestations, viral encephalitis is often confused with other central nervous system diseases. In this case, we reported a young male patient who was admitted to the hospital chiefly complaining of “diplopia for more than two months and aggravated walking instability for more than 10 days”. After admission, relevant patient blood and cerebrospinal fluid (CSF) tests were completed, and no obvious abnormalities were found. Chest CT suggested pulmonary infection; magnetic resonance imaging (MRI) and contrast-enhanced CT, PET-CT and other imaging examinations of the head all indicated a high possibility of viral encephalitis. Symptoms of fever were improved in the patient after treatment with antiviral therapy and anti-infection therapy. However, symptoms of neurological function loss, such as double vision and adverse right limb movement, persisted. Finally, stereotactic biopsies of deep brain lesions were carried out and sent to the pathology department, which led to a diagnosis of diffuse midline glioma, H3K27M-mutant subtype (WHO IV). His family chose to perform conservative treatment in another hospital, and the patient died four months later. To conclude, when clinical symptoms of suspected viral encephalitis appear in the course of diffuse midline glioma, it can result in confusion regarding clinical diagnosis and treatment. Clinicians should ensure proper early recognition and identification of the disease.

scholarly journals Small Maf Compound Mutants Display Central Nervous System Neuronal Degeneration, Aberrant Transcription, and Bach Protein Mislocalization Coincident with Myoclonus and Abnormal Startle Response

2003 ◽  
Vol 23 (4) ◽  
pp. 1163-1174 ◽  
Author(s):  
Fumiki Katsuoka ◽  
Hozumi Motohashi ◽  
Yuna Tamagawa ◽  
Shigeo Kure ◽  
Kazuhiko Igarashi ◽  
...  
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Germ Line ◽  
Neuronal Degeneration ◽  
Gene Dosage ◽  
Morphological Changes ◽  
Glycine Receptor ◽  
Neurological Dysfunction ◽  
Transcriptional Responses ◽  
Nuclear Extracts

ABSTRACT The small Maf proteins form heterodimers with CNC and Bach family proteins to elicit transcriptional responses from Maf recognition elements (MAREs). We previously reported germ line-targeted deficiencies in mafG plus mafK compound mutant mice. The most prominent mutant phenotype was a progressive maf dosage-dependent neuromuscular dysfunction. However, there has been no previous report regarding the effects of altered small-maf gene expression on neurological dysfunction. We show here that MafG and MafK are expressed in discrete central nervous system (CNS) neurons and that mafG::mafK compound mutants display neuronal degeneration coincident with surprisingly selective MARE-dependent transcriptional abnormalities. The CNS morphological changes are concurrent with the onset of a neurological disorder in the mutants, and the behavioral changes are accompanied by reduced glycine receptor subunit accumulation. Bach/small Maf heterodimers, which normally generate transcriptional repressors, were significantly underrepresented in nuclear extracts prepared from maf mutant brains, and Bach proteins fail to accumulate normally in nuclei. Thus compound mafG::mafK mutants develop age- and maf gene dosage-dependent cell-autonomous neuronal deficiencies that lead to profound neurological defects.

Neurotropic enteroviruses co-opt “fair-weather-friend” commensal gut microbiota to drive host infection and central nervous system disturbances

2019 ◽  
Vol 42 ◽  
Author(s):  
Kevin B. Clark
Keyword(s):  
Central Nervous System ◽  
Nervous System ◽  
Gut Bacteria ◽  
Infection Cycle ◽  
Fair Weather ◽  
Host Health ◽  
Microbe Interactions ◽  
Animal Hosts ◽  
Host Infection ◽  
Neuropsychiatric Conditions

Abstract Some neurotropic enteroviruses hijack Trojan horse/raft commensal gut bacteria to render devastating biomimicking cryptic attacks on human/animal hosts. Such virus-microbe interactions manipulate hosts’ gut-brain axes with accompanying infection-cycle-optimizing central nervous system (CNS) disturbances, including severe neurodevelopmental, neuromotor, and neuropsychiatric conditions. Co-opted bacteria thus indirectly influence host health, development, behavior, and mind as possible “fair-weather-friend” symbionts, switching from commensal to context-dependent pathogen-like strategies benefiting gut-bacteria fitness.

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