scholarly journals Impact of Ultrabithorax alternative splicing on Drosophila embryonic nervous system development

2015 ◽  
Vol 138 ◽  
pp. 177-189 ◽  
Author(s):  
Aenne Geyer ◽  
Ioanna Koltsaki ◽  
Christian Hessinger ◽  
Simone Renner ◽  
Ana Rogulja-Ortmann
Keyword(s):  
Nervous System ◽  
Alternative Splicing ◽  
System Development ◽  
Nervous System Development ◽  
Embryonic Nervous System

scholarly journals RNA interference screen to identify genes required for Drosophila embryonic nervous system development

2007 ◽  
Vol 104 (13) ◽  
pp. 5626-5631 ◽  
Author(s):  
K. Koizumi ◽  
H. Higashida ◽  
S. Yoo ◽  
M. S. Islam ◽  
A. I. Ivanov ◽  
...  
Keyword(s):  
Nervous System ◽  
Rna Interference ◽  
System Development ◽  
Nervous System Development ◽  
Embryonic Nervous System

scholarly journals Noninvasive harmonics optical microscopy for long-term observation of embryonic nervous system development in vivo

2006 ◽  
Vol 11 (5) ◽  
pp. 054022 ◽  
Author(s):  
Szu-Yu Chen ◽  
Cho-Shuen Hsieh ◽  
Shi-Wei Chu ◽  
Cheng-Yung Lin ◽  
Ching-Yi Ko ◽  
...  
Keyword(s):  
Nervous System ◽  
Optical Microscopy ◽  
System Development ◽  
Nervous System Development ◽  
Embryonic Nervous System ◽  
Long Term Observation

Genetic analysis of vein function in the Drosophila embryonic nervous system

Genome ◽  
2000 ◽  
Vol 43 (3) ◽  
pp. 564-573 ◽  
Author(s):  
Bradley R Lanoue ◽  
Michael D Gordon ◽  
Robin Battye ◽  
J Roger Jacobs
Keyword(s):  
Nervous System ◽  
Egf Receptor ◽  
System Development ◽  
Cell Lineage ◽  
Growth Factor Receptor ◽  
Neuronal Cell ◽  
Cell Number ◽  
Nervous System Development ◽  
Egfr Signaling ◽  
Embryonic Nervous System

The Drosophila epidermal growth factor receptor (EGFR) may be activated by two ligands expressed in the embryonic nervous system, Spitz and Vein. Previous studies have established Spitz as an essential activator of EGFR signaling in nervous system development. Here, we report the pattern of expression of vein mRNA in the nervous system and characterize the contribution of vein to cell lineage and axonogenesis. The number of midline glia (MG) precursors is reduced in vein mutants before the onset of embryonic apoptosis. In contrast to spitz, mis-expression of vein does not suppress apoptosis in the MG. These data indicate that early midline EGFR signaling, requiring vein and spitz, establishes MG precursor number, whereas later EGFR signals, requiring spitz, suppress apoptosis in the MG. vein mutants show early irregularities during axon tract establishment, which resolve later to variable defasciculation and thinner intersegmental axon tracts. vein and spitz phenotypes act additively in the regulation of MG cell number, but show synergism in a midline neuronal cell number phenotype and in axon tract architecture. vein appears to act downstream of spitz to briefly amplify local EGFR activation.Key words: Drosophila, vein, midline, axonogenesis, EGF receptor, lineage, neuregulin, spitz, CNS.

Signaling in glial development: differentiation migration and axon guidance

2004 ◽  
Vol 82 (6) ◽  
pp. 694-707 ◽  
Author(s):  
Robert J Parker ◽  
Vanessa J Auld
Keyword(s):  
Nervous System ◽  
Axon Guidance ◽  
Egf Receptor ◽  
System Development ◽  
Molecular Genetic ◽  
Model Organism ◽  
Cell Types ◽  
Nervous System Development ◽  
Glial Development ◽  
Embryonic Nervous System

Glial cells have diverse functions that are necessary for the proper development and function of complex nervous systems. During development, a variety of reciprocal signaling interactions between glia and neurons dictate all parts of nervous system development. Glia may provide attractive, repulsive, or contact-mediated cues to steer neuronal growth cones and ensure that neurons find their appropriate synaptic targets. In fact, both neurons and glia may act as migrational substrates for one another at different times during development. Also, the exchange of trophic signals between glia and neurons is essential for the proper bundling, fasciculation, and ensheathement of axons as well as the differentiation and survival of both cell types. The growing number of links between glial malfunction and human disease has generated great interest in glial biology. Because of its relative simplicity and the many molecular genetic tools available, Drosophila is an excellent model organism for studying glial development. This review will outline the roles of glia and their interactions with neurons in the embryonic nervous system of the fly.Key words: glia, axon guidance, migration, EGF receptor.

scholarly journals Deficiency of Pro-apoptotic Hrk Attenuates Programmed Cell Death in the Developing Murine Nervous System but Does Not Affect Bcl-x Deficiency-Induced Neuron Apoptosis

2011 ◽  
Vol 59 (11) ◽  
pp. 976-983 ◽  
Author(s):  
Arindam P. Ghosh ◽  
Jennifer D. Cape ◽  
Barbara J. Klocke ◽  
Kevin A. Roth
Keyword(s):  
Cell Death ◽  
Nervous System ◽  
Programmed Cell Death ◽  
System Development ◽  
Critical Role ◽  
Family Members ◽  
Nervous System Development ◽  
Neuronal Populations ◽  
Embryonic Nervous System ◽  
Induced Neuron

The BCL-2 family includes both pro- and anti-apoptotic proteins, which regulate programmed cell death during development and in response to various apoptotic stimuli. The BH3-only subgroup of pro-apoptotic BCL-2 family members is critical for the induction of apoptotic signaling, by binding to and neutralizing anti-apoptotic BCL-2 family members. During embryonic development, the anti-apoptotic protein BCL-XL plays a critical role in the survival of neuronal populations by regulating the multi-BH domain protein BAX. In this study, the authors investigated the role of Harakiri (HRK), a relatively recently characterized BH3-only molecule in disrupting the BAX-BCL-XL interaction during nervous system development. Results indicate that HRK deficiency significantly reduces programmed cell death in the nervous system. However, HRK deficiency does not significantly attenuate the widespread apoptosis seen in the Bcl-x−/− embryonic nervous system, indicating that other BH3-only molecules, alone or in combination, may regulate BAX activation in immature neurons.

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