Files in this item
|(no description provided)|
|Title:||Neuroblast lineage and cell fate specification in the Drosophila central nervous system|
|Doctoral Committee Chair(s):||Doe, Chris Q.|
|Department / Program:||Biology, Molecular
|Degree Granting Institution:||University of Illinois at Urbana-Champaign|
|Abstract:||The generation of cellular diversity during early development of nervous system is poorly understood. In the Drosophila central nervous system, cell diversity is primarily generated by the invariant lineage of neural precursors called neuroblasts. It has been proposed that a class of genes are expressed in neuroblasts and their progeny and control the cell lineage of each neuroblast.
I used an enhancer trap screen to identify the ming gene, which is transiently expressed in a subset of neuroblasts at reproducible points in their cell lineage (i.e. in neuroblast sublineages), suggesting that neuroblast identity can be altered during its cell lineage. ming encodes a predicted zinc finger protein within the TFIIIA superfamily. Loss of ming function results in altered CNS expression of the engrailed gene, defects in axonogenesis and embryonic lethality. I propose that ming, as a neuroblast sublineage gene, controls distinct cell fates within neuroblast cell lineages.
I investigate the precise temporal regulation of the sublineage gene expression. I show that four genes (ming, even-skipped, unplugged and achaete) are expressed in specific neuroblast sublineages. I show that these neuroblasts can be identified in embryos lacking both neuroblast cytokinesis and cell cycle progression (string mutants) and in embryos lacking only neuroblast cytokinesis (pebble mutants). I find that the unplugged and achaete genes are expressed normally in string and pebble mutant embryos, indicating that temporal control is independent of neuroblast cytokinesis or counting cell cycles. In contrast, neuroblasts require cytokinesis to activate sublineage ming expression, while a single, identified neuroblast requires cell cycle progression to activate even-skipped expression. These results suggest that neuroblasts have an intrinsic gene regulatory hierarchy controlling unplugged and achaete expression, but that cell cycle- or cytokinesis-dependent mechanisms are required for ming and eve CNS expression.
|Rights Information:||Copyright 1995 Cui, Xuan|
|Date Available in IDEALS:||2011-05-07|
|Identifier in Online Catalog:||AAI9624328|