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

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.

2004 ◽  
Vol 82 (6) ◽  
pp. 694-707 ◽  
Author(s):  
Robert J Parker ◽  
Vanessa J Auld

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.


2007 ◽  
Vol 104 (13) ◽  
pp. 5626-5631 ◽  
Author(s):  
K. Koizumi ◽  
H. Higashida ◽  
S. Yoo ◽  
M. S. Islam ◽  
A. I. Ivanov ◽  
...  

2006 ◽  
Vol 11 (5) ◽  
pp. 054022 ◽  
Author(s):  
Szu-Yu Chen ◽  
Cho-Shuen Hsieh ◽  
Shi-Wei Chu ◽  
Cheng-Yung Lin ◽  
Ching-Yi Ko ◽  
...  

2020 ◽  
Vol 10 (6) ◽  
pp. 1949-1962 ◽  
Author(s):  
Elyse L. Christensen ◽  
Alexandra Beasley ◽  
Jessica Radchuk ◽  
Zachery E. Mielko ◽  
Elicia Preston ◽  
...  

Proper nervous system development is required for an organism’s survival and function. Defects in neurogenesis have been linked to neurodevelopmental disorders such as schizophrenia and autism. Understanding the gene regulatory networks that orchestrate neural development, specifically cascades of proneural transcription factors, can better elucidate which genes are most important during early neurogenesis. Neurogenins are a family of deeply conserved factors shown to be both necessary and sufficient for the development of neural subtypes. However, the immediate downstream targets of neurogenin are not well characterized. The objective of this study was to further elucidate the role of ngn-1/neurogenin in nervous system development and to identify its downstream transcriptional targets, using the nematode Caenorhabditis elegans as a model for this work. We found that ngn-1 is required for axon outgrowth, nerve ring architecture, and neuronal cell fate specification. We also showed that ngn-1 may have roles in neuroblast migration and epithelial integrity during embryonic development. Using RNA sequencing and comparative transcriptome analysis, we identified eight transcription factors (hlh-34/NPAS1, unc-42/PROP1, ceh-17/PHOX2A, lim-4/LHX6, fax-1/NR2E3, lin-11/LHX1, tlp-1/ZNF503, and nhr-23/RORB) whose transcription is activated, either directly or indirectly, by ngn-1. Our results show that ngn-1 has a role in transcribing known terminal regulators that establish and maintain cell fate of differentiated neural subtypes and confirms that ngn-1 functions as a proneural transcription factor in C. elegans neurogenesis.


eLife ◽  
2016 ◽  
Vol 5 ◽  
Author(s):  
Johannes Stratmann ◽  
Hugo Gabilondo ◽  
Jonathan Benito-Sipos ◽  
Stefan Thor

During Drosophila embryonic nervous system development, neuroblasts express a programmed cascade of five temporal transcription factors that govern the identity of cells generated at different time-points. However, these five temporal genes fall short of accounting for the many distinct cell types generated in large lineages. Here, we find that the late temporal gene castor sub-divides its large window in neuroblast 5–6 by simultaneously activating two cell fate determination cascades and a sub-temporal regulatory program. The sub-temporal program acts both upon itself and upon the determination cascades to diversify the castor window. Surprisingly, the early temporal gene Kruppel acts as one of the sub-temporal genes within the late castor window. Intriguingly, while the temporal gene castor activates the two determination cascades and the sub-temporal program, spatial cues controlling cell fate in the latter part of the 5–6 lineage exclusively act upon the determination cascades.


2011 ◽  
Vol 59 (11) ◽  
pp. 976-983 ◽  
Author(s):  
Arindam P. Ghosh ◽  
Jennifer D. Cape ◽  
Barbara J. Klocke ◽  
Kevin A. Roth

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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