FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Li, Q.J., Pazdera, T.M., Minden, J.S. (1999). Drosophila embryonic pattern repair: how embryos respond to cyclin E-induced ectopic division.  Development 126(10): 2299--2307.
FlyBase ID
FBrf0108433
Publication Type
Research paper
Abstract
The Drosophila melanogaster embryo ordinarily undergoes thirteen cycles of rapid syncytial division followed by three rounds of cellular division for most cells. Strict regulation of the number of divisions is believed to be essential for normal patterning and development. To determine how the embryo responds to hyperplastic growth, we have examined epidermal development in embryos that experience additional rounds of mitosis as the result of ectopic Cyclin E expression. We observed that the cell density in the epidermis nearly doubled within 1 hour of Cyclin E induction. The spacing and width of the ENGRAILED and wingless stripes was unchanged, but the cell density within the stripes was increased. By 4 hours after Cyclin E induction, the cell density had returned to almost normal values. The embryos developed, albeit more slowly, to produce viable larvae and adults. The excess cells were removed by apoptosis in a reaper-dependent fashion as evidenced by increased reaper expression. Embryos lacking cell death in the abdomen exhibited changes in ENGRAILED expression. In addition, germband retraction and dorsal closure were slower than normal. Ectopic Cyclin E expression in cell-death-deficient embryos exacerbated the germband retraction and ENGRAILED-expression defects.
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    Language of Publication
    English
    Additional Languages of Abstract
    Parent Publication
    Publication Type
    Journal
    Abbreviation
    Development
    Title
    Development
    Publication Year
    1987-
    ISBN/ISSN
    0950-1991
    Data From Reference
    Aberrations (2)
    Alleles (1)
    Genes (4)
    Transgenic Constructs (1)