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The commonly used marker ELAV is transiently expressed in neuroblasts and glial cells in the Drosophila embryonic CNS.

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TLDR
In the embryo, elav can no longer be considered an exclusive marker or driver for postmitotic neurons and elav loss‐of‐function mutants show no obvious effects on the number and pattern of embryonic glia.
Abstract
Glial cells in the Drosophila embryonic nervous system can be monitored with the marker Reversed-polarity (Repo), whereas neurons lack Repo and express the RNA-binding protein ELAV (Embryonic Lethal, Abnormal Vision). Since the first description of the ELAV protein distribution in 1991 (Robinow and White), it is believed that ELAV is an exclusive neuronal and postmitotic marker. Looking at ELAV expression, we unexpectedly observed that, in addition to neurons, ELAV is transiently expressed in embryonic glial cells. Furthermore, it is transiently present in the proliferating longitudinal glioblast, and it is transcribed in embryonic neuroblasts. Likewise, elav-Gal4 lines, which are generally used as postmitotic neuronal driver lines, show expression in neural progenitor cells and nearly all embryonic glial cells. Thus, in the embryo, elav can no longer be considered an exclusive marker or driver for postmitotic neurons. elav loss-of-function mutants show no obvious effects on the number and pattern of embryonic glia.

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Citations
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Journal ArticleDOI

Allatostatin A Signalling in Drosophila Regulates Feeding and Sleep and Is Modulated by PDF

TL;DR: It is suggested that pleiotropic AstA signalling by a distinct neuronal and enteroendocrine AstA cell subset adapts the fly to a digestive energy-saving state which can be modulated by PDF.
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ELAV mediates 3′ UTR extension in the Drosophila nervous system

TL;DR: RNA immunoprecipitation assays suggest that ELAV directly binds the proximal polyadenylation signals of many target mRNAs, and it is proposed that this mechanism for coordinating 3' UTR extension may be generally used in a variety of cellular processes.
Journal ArticleDOI

Differential Effects of Tau on the Integrity and Function of Neurons Essential for Learning in Drosophila

TL;DR: The data support the notion that phosphorylation at particular sites rather than hyperphosphorylation per se mediates toxicity or dysfunction in a cell type-specific manner.
References
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Journal ArticleDOI

Distinct morphogenetic functions of similar small GTPases: Drosophila Drac1 is involved in axonal outgrowth and myoblast fusion.

TL;DR: Cloned Drosophila homologs of rac and CDC42, Drac1, and Dcdc42 proteins cause qualitatively distinct morphological defects, suggesting that similar GTPases in the same subfamily have unique roles in morphogenesis.
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Asymmetric Segregation of the Tumor Suppressor Brat Regulates Self-Renewal in Drosophila Neural Stem Cells

TL;DR: It is shown that Drosophila larval neuroblasts-stem cell-like precursors of the adult brain-regulate proliferation by segregating the growth inhibitor Brat and the transcription factor Prospero into only one daughter cell.
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Characterization and spatial distribution of the ELAV protein during Drosophila melanogaster development.

TL;DR: It is proposed that the elav gene provides a neuronal-housekeeping function that is required for the successful posttranscriptional processing of transcripts from a set of genes the function of which is requiredfor proper neuronal development and maintenance.
Journal ArticleDOI

Characterization and localization of the even-skipped protein of Drosophila.

TL;DR: The pair‐rule gene even‐skipped of Drosophila is isolated and it is shown that the eve protein is distributed in a series of seven transverse stripes at the cellular blastoderm stage, and is localized primarily within the nuclear regions of those embryonic cells that express the gene.
Journal ArticleDOI

glial cells missing: a genetic switch that controls glial versus neuronal fate.

TL;DR: The glial cells missing (gcm) gene in Drosophila encodes a novel nuclear protein that is transiently expressed early in the development of nearly all glia, and appears to function as a binary genetic switch for glia versus neurons.
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