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Citation
Certel, S.J., Johnson, W.A. (1996). Disruption of mesectodermal lineages by temporal misexpression of the Drosophila POU-domain transcription factor, drifter.  Dev. Genet. 18(4): 279--288.
FlyBase ID
FBrf0089611
Publication Type
Research paper
Abstract
Among the first cells to differentiate in the Drosophila ventral nerve cord, the mesectodermal (midline) lineage gives rise to a discrete set of neurons and glia previously demonstrated to play an important role in the organization of the developing nervous system. The relative simplicity of the midline has allowed the elucidation of many aspects of initial lineage commitment and subsequent differentiation. Based upon its mesectodermal expression pattern and loss-of-function phenotype, we have proposed a key role for the Drosophila POU-domain transcription factor, drifter (dfr), in mesectodermal lineage development. In this study, we have examined the developmental consequences of dfr misexpression using transgenic lines expressing wild-type Drifter protein under control of the heat-inducible hsp70 promoter. Induction of ubiquitous DFR protein during a restricted period of embryogenesis causes a defective axonal phenotype characterized by failure of commissure formation. Based on examination of cell-specific markers for mesectodermal cells, these defects appear to be the result of a suppression of single-minded expression resulting in the disruption of mesectodermal lineage designation and differentiation. The observed temporally restricted sensitivity to DFR expression suggests possible interactions between DFR protein and other stage-specific mesectodermal regulatory factors present before or after a defined mesectodermal developmental event.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Dev. Genet.
    Title
    Developmental Genetics
    Publication Year
    1979-1999
    ISBN/ISSN
    0192-253X
    Data From Reference
    Aberrations (1)
    Alleles (6)
    Balancers (1)
    Genes (8)
    Insertions (4)
    Transgenic Constructs (1)