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Developmental control of neuronal survival in the Drosophila embryonic central nervous system

This work concerns the roles of neuron glia interactions in the control of neuronal survival during Central Nervous System (CNS) development in <I>Drosophila. </I>The question of whether glia are required to maintain neuronal survival in insects was addressed. Firstly, the GAL4 system was used to achieve in vivo targeted genetic ablation of glia. Secondly, plasmid rescue and P-element excision were exploited to locate and mutate genes which might participate in neuron glia interactions. Targeted glial ablation did not affect pioneer neuron survival. However, increased apoptosis was observed among the FasII and 22C10 expressing subsets of the follower neurons. Targeted ablation only of the interface glia was sufficient to induce follower neuron apoptosis. This difference in the survival requirements of pioneer and follower neurons may be instructive in patterning of the CNS. Neuronal apoptosis was rescued by ablating glia in an apoptosis deficient genetic background, and by expressing the <I>p35</I> apoptosis inhibitor under the neural <I>elav</I> promoter. Hence the loss of neighbouring glia induces nonautonomous neuronal apoptosis. The <I>Mz1131</I> enhancer-trap line, expressed in the interface glia, was used to examine the effects of mutating a putative glial gene upon CNS development. Lethal <I>Mz1131</I> mutants displayed increased apoptosis of lateral glia and FasII expressing neurons, but not of 22C10 expressing neurons. The fasciculation and defasciculation of the longitudinal axon tracts as also affected. Both lethality and the characteristic GAL4 expression pattern of <I>Mz1131</I> were lost upon P-element excision. Nonradioactive southern blotting revealed that line <I>Mz1131</I> contains multiple P-insertions. Identification of sequences neighbouring P-insertions, and complementation tests revealed a mutation at the <I>sin3A </I>locus.

Identiferoai:union.ndltd.org:bl.uk/oai:ethos.bl.uk:596769
Date January 2002
CreatorsBooth, G. E.
PublisherUniversity of Cambridge
Source SetsEthos UK
Detected LanguageEnglish
TypeElectronic Thesis or Dissertation

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