scholarly journals 09-P058 The role of the forkhead gene fd3F in Drosophila chordotonal neuron development

2009 ◽  
Vol 126 ◽  
pp. S167
Author(s):  
Fay Newton ◽  
Andrew Jarman
Keyword(s):  
Neuron Development ◽  
Forkhead Gene

The role of Ret receptor tyrosine kinase in dopaminergic neuron development

Neuroscience ◽  
2006 ◽  
Vol 142 (2) ◽  
pp. 391-400 ◽  
Author(s):  
L. Li ◽  
Y. Su ◽  
C. Zhao ◽  
H. Zhao ◽  
G. Liu ◽  
...  
Keyword(s):  
Tyrosine Kinase ◽  
Receptor Tyrosine Kinase ◽  
Dopaminergic Neuron ◽  
Neuron Development

scholarly journals sli is required for proper morphology and migration of sensory neurons in the Drosophila PNS

2019 ◽  
Vol 14 (1) ◽  
Author(s):  
Madison Gonsior ◽  
Afshan Ismat
Keyword(s):  
Nervous System ◽  
Sensory Neurons ◽  
Glial Cells ◽  
System Development ◽  
Nervous System Development ◽  
Final Position ◽  
Neuron Development ◽  
Guidance Cues ◽  
And Migration

Abstract Neurons and glial cells coordinate with each other in many different aspects of nervous system development. Both types of cells are receiving multiple guidance cues to guide the neurons and glial cells to their proper final position. The lateral chordotonal organs (lch5) of the Drosophila peripheral nervous system (PNS) are composed of five sensory neurons surrounded by four different glial cells, scolopale cells, cap cells, attachment cells and ligament cells. During embryogenesis, the lch5 neurons go through a rotation and ventral migration to reach their final position in the lateral region of the abdomen. We show here that the extracellular ligand sli is required for the proper ventral migration and morphology of the lch5 neurons. We further show that mutations in the Sli receptors Robo and Robo2 also display similar defects as loss of sli, suggesting a role for Slit-Robo signaling in lch5 migration and positioning. Additionally, we demonstrate that the scolopale, cap and attachment cells follow the mis-migrated lch5 neurons in sli mutants, while the ventral stretching of the ligament cells seems to be independent of the lch5 neurons. This study sheds light on the role of Slit-Robo signaling in sensory neuron development.

scholarly journals An Emerging Role of m6A in Memory: A Case for Translational Priming

2020 ◽  
Vol 21 (20) ◽  
pp. 7447
Author(s):  
Amanda M. Leonetti ◽  
Ming Yin Chu ◽  
Fiona O. Ramnaraign ◽  
Samuel Holm ◽  
Brandon J. Walters
Keyword(s):  
Learning And Memory ◽  
Memory Consolidation ◽  
Protein Translation ◽  
Memory Formation ◽  
Current Data ◽  
Neuron Development ◽  
Neuronal Functions ◽  
The Brain ◽  
Fine Tune

Investigation into the role of methylation of the adenosine base (m6A) of RNA has only recently begun, but it quickly became apparent that m6A is able to control and fine-tune many aspects of mRNA, from splicing to translation. The ability of m6A to regulate translation distally, away from traditional sites near the nucleus, quickly caught the eye of neuroscientists because of implications for selective protein translation at synapses. Work in the brain has demonstrated how m6A is functionally required for many neuronal functions, but two in particular are covered at length here: The role of m6A in 1) neuron development; and 2) memory formation. The purpose of this review is not to cover all data about m6A in the brain. Instead, this review will focus on connecting mechanisms of m6A function in neuron development, with m6A’s known function in memory formation. We will introduce the concept of “translational priming” and discuss how current data fit into this model, then speculate how m6A-mediated translational priming during memory consolidation can regulate learning and memory locally at the synapse.

scholarly journals Critical role of TRPC1 in thyroid hormone-dependent dopaminergic neuron development

2017 ◽  
Vol 1864 (10) ◽  
pp. 1900-1912 ◽  
Author(s):  
Chunhai Chen ◽  
Qinglong Ma ◽  
Ping Deng ◽  
Jianjing Yang ◽  
Lingling Yang ◽  
...  
Keyword(s):  
Thyroid Hormone ◽  
Dopaminergic Neuron ◽  
Critical Role ◽  
Neuron Development

scholarly journals Orexin/Hypocretin and Histamine Cross-Talk on Hypothalamic Neuron Counts in Mice

2021 ◽  
Vol 15 ◽  
Author(s):  
Chiara Berteotti ◽  
Viviana Lo Martire ◽  
Sara Alvente ◽  
Stefano Bastianini ◽  
Cristiano Bombardi ◽  
...  
Keyword(s):  
Histidine Decarboxylase ◽  
Neuron Development ◽  
Wild Type ◽  
Hypothalamic Neurons ◽  
Neuron Number ◽  
Knock Out ◽  
Orexin Neuron ◽  
Knock Out Mice ◽  
Deficient Mice

The loss of hypothalamic neurons that produce wake-promoting orexin (hypocretin) neuropeptides is responsible for narcolepsy type 1 (NT1). While the number of histamine neurons is increased in patients with NT1, results on orexin-deficient mouse models of NT1 are inconsistent. On the other hand, the effect of histamine deficiency on orexin neuron number has never been tested on mammals, even though histamine has been reported to be essential for the development of a functional orexin system in zebrafish. The aim of this study was to test whether histamine neurons are increased in number in orexin-deficient mice and whether orexin neurons are decreased in number in histamine-deficient mice. The hypothalamic neurons expressing L-histidine decarboxylase (HDC), the histamine synthesis enzyme, and those expressing orexin A were counted in four orexin knock-out mice, four histamine-deficient HDC knock-out mice, and four wild-type C57BL/6J mice. The number of HDC-positive neurons was significantly higher in orexin knock-out than in wild-type mice (2,502 ± 77 vs. 1,800 ± 213, respectively, one-tailed t-test, P = 0.011). Conversely, the number of orexin neurons was not significantly lower in HDC knock-out than in wild-type mice (2,306 ± 56 vs. 2,320 ± 120, respectively, one-tailed t-test, P = 0.459). These data support the view that orexin peptide deficiency is sufficient to increase histamine neuron number, supporting the involvement of the histamine waking system in the pathophysiology of NT1. Conversely, these data do not support a significant role of histamine in orexin neuron development in mammals.

scholarly journals Molecular Regulation in Dopaminergic Neuron Development. Cues to Unveil Molecular Pathogenesis and Pharmacological Targets of Neurodegeneration

2020 ◽  
Vol 21 (11) ◽  
pp. 3995 ◽  
Author(s):  
Floriana Volpicelli ◽  
Carla Perrone-Capano ◽  
Gian Carlo Bellenchi ◽  
Luca Colucci-D’Amato ◽  
Umberto di Porzio
Keyword(s):  
Dopaminergic Neurons ◽  
Posttranscriptional Regulation ◽  
Gene Network ◽  
Molecular Pathogenesis ◽  
Mammalian Brain ◽  
Neuron Development ◽  
Pharmacological Targets ◽  
Neuropsychiatric Diseases ◽  
And Function

The relatively few dopaminergic neurons in the mammalian brain are mostly located in the midbrain and regulate many important neural functions, including motor integration, cognition, emotive behaviors and reward. Therefore, alteration of their function or degeneration leads to severe neurological and neuropsychiatric diseases. Unraveling the mechanisms of midbrain dopaminergic (mDA) phenotype induction and maturation and elucidating the role of the gene network involved in the development and maintenance of these neurons is of pivotal importance to rescue or substitute these cells in order to restore dopaminergic functions. Recently, in addition to morphogens and transcription factors, microRNAs have been identified as critical players to confer mDA identity. The elucidation of the gene network involved in mDA neuron development and function will be crucial to identify early changes of mDA neurons that occur in pre-symptomatic pathological conditions, such as Parkinson’s disease. In addition, it can help to identify targets for new therapies and for cell reprogramming into mDA neurons. In this essay, we review the cascade of transcriptional and posttranscriptional regulation that confers mDA identity and regulates their functions. Additionally, we highlight certain mechanisms that offer important clues to unveil molecular pathogenesis of mDA neuron dysfunction and potential pharmacological targets for the treatment of mDA neuron dysfunction.

A forkhead gene related to HNF-3beta is required for gastrulation and axis formation in the ascidian embryo

Development ◽  
1997 ◽  
Vol 124 (18) ◽  
pp. 3609-3619 ◽  
Author(s):  
C.L. Olsen ◽  
W.R. Jeffery
Keyword(s):  
Muscle Cells ◽  
Single Copy ◽  
The Body ◽  
Axis Formation ◽  
Vegetal Pole ◽  
Tailbud Stage ◽  
Notochord Cells ◽  
Mesenchyme Cells ◽  
Forkhead Gene

We have isolated a member of the HNF-3/forkhead gene family in ascidians as a means to determine the role of winged-helix genes in chordate development. The MocuFH1 gene, isolated from a Molgula oculata cDNA library, exhibits a forkhead DNA-binding domain most similar to zebrafish axial and rodent HNF-3beta. MocuFH1 is a single copy gene but there is at least one other related forkhead gene in the M. oculata genome. The MocuFH1 gene is expressed in the presumptive endoderm, mesenchyme and notochord cells beginning during the late cleavage stages. During gastrulation, MocuFH1 expression occurs in the prospective endoderm cells, which invaginate at the vegetal pole, and in the presumptive notochord and mesenchyme cells, which involute over the anterior and lateral lips of the blastopore, respectively. However, this gene is not expressed in the presumptive muscle cells, which involute over the posterior lip of the blastopore. MocuFH1 expression continues in the same cell lineages during neurulation and axis formation, however, during the tailbud stage, MocuFH1 is also expressed in ventral cells of the brain and spinal cord. The functional role of the MocuFH1 gene was studied using antisense oligodeoxynucleotides (ODNs), which transiently reduce MocuFH1 transcript levels during gastrulation. Embryos treated with antisense ODNs cleave normally and initiate gastrulation. However, gastrulation is incomplete, some of the endoderm and notochord cells do not enter the embryo and undergo subsequent movements, and axis formation is abnormal. In contrast, the prospective muscle cells, which do not express MocuFH1, undergo involution and later express muscle actin and acetylcholinesterase, markers of muscle cell differentiation. The results suggest that MocuFH1 is required for morphogenetic movements of the endoderm and notochord precursor cells during gastrulation and axis formation. The effects of inhibiting MocuFH1 expression on embryonic axis formation in ascidians are similar to those reported for knockout mutations of HNF-3beta in the mouse, suggesting that HNF-3/forkhead genes have an ancient and fundamental role in organizing the body plan in chordates.

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