Rab11 is required for embryonic nervous system development in Drosophila

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.

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Signaling in glial development: differentiation migration and axon guidance

Biochemistry and Cell Biology ◽

10.1139/o04-119 ◽

2004 ◽

Vol 82 (6) ◽

pp. 694-707 ◽

Cited By ~ 14

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.

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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

Journal of Histochemistry & Cytochemistry ◽

10.1369/0022155411424311 ◽

2011 ◽

Vol 59 (11) ◽

pp. 976-983 ◽

Cited By ~ 7

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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