Delamination and division in the Drosophila neurectoderm: spatiotemporal pattern, cytoskeletal dynamics, and common control by neurogenic and segment polarity genes.
Cytoskeletal changes occurring during the delamination of precursors of the peripheral (microchaete precursors in the pupal notum) and central nervous system (embryonic SI neuroblasts) were studied. The pattern of cell division in the ventral neurectoderm (VN) of wild-type embryos was analyzed using BrdU incorporation and correlated to the pattern of neuroblast delamination. Finally, defects in the pattern of proliferation of the VN and neuroblast delamination which occur in Notch and wingless mutant embryos were described. The results indicate that the patterns of delamination and mitosis are closely correlated: delamination occurs either immediately after a cell has divided (in case of microchaete precursors) or shortly before the division (in case of the neuroblasts). In addition, cytoskeletal changes similar to those occurring during mitosis can be seen in delaminating neuronal precursors. Thus, during both mitosis and delamination, the discrete apicobasally oriented microfilament-tubulin bundles break down. Microfilaments form a dense, diffuse cortical layer surrounding the entire cell body. Microtubules are concentrated at the apically located centrosome. The relationship between mitosis and delamination is supported by the finding that the neurogenic gene Notch and segment polarity gene wingless (wg) affect both proliferation and delamination in the ventral neurectoderm. Thus, in embryos expressing the trunkated cytoplasmic domain of the neurogenic gene Notch under heat-shock control (Struhl et al., 1993), all ventral neurectodermal cells go into mitosis prematurely, followed by the absence of neuroblast delamination. In wg loss-of-function mutants, mitosis in the VN is irregular and generally postponed, accompanied by irregularities in the timing of neuroblast delamination in general and the absence of a subset of neuroblasts.
Department of Biology, University of California Los Angeles 90024.
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Hartenstein
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Younossi-Hartenstein
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Lekven
D008841:Actin Cytoskeleton / Q000502:physiology; D000818:Animals; D002455:Cell Division; D002465:Cell Movement; D029721:Drosophila Proteins; D004331:Drosophila melanogaster / Q000196:embryology; D004475:Ectoderm / Q000166:cytology; D004847:Epithelial Cells; D007301:Insect Hormones / Q000502:physiology*; D008565:Membrane Proteins / Q000502:physiology*; D008870:Microtubules / Q000502:physiology; D008938:Mitosis; D009024:Morphogenesis; D009420:Nervous System / Q000196:embryology*; D009474:Neurons / Q000166:cytology; D011518:Proto-Oncogene Proteins / Q000502:physiology*; D051880:Receptors, Notch; D051155:Wnt1 Protein
D029721:Drosophila Proteins; D007301:Insect Hormones; D008565:Membrane Proteins; C497759:N protein, Drosophila; D011518:Proto-Oncogene Proteins; D051880:Receptors, Notch; D051155:Wnt1 Protein; C074622:wg protein, Drosophila