FB2026_01 , released March 12, 2026
FB2026_01 , released March 12, 2026
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Citation
Davis, T.L., Rebay, I. (2017). Antagonistic regulation of the second mitotic wave by Eyes absent-Sine oculis and Combgap coordinates proliferation and specification in the Drosophila retina.  Development 144(14): 2640--2651.
FlyBase ID
FBrf0236135
Publication Type
Research paper
Abstract
The transition from proliferation to specification is fundamental to the development of appropriately patterned tissues. In the developing Drosophila eye, Eyes absent (Eya) and Sine oculis (So) orchestrate the progression of progenitor cells from asynchronous cell division to G1 arrest and neuronal specification at the morphogenetic furrow. Here, we uncover a novel role for Eya and So in promoting cell cycle exit in the second mitotic wave (SMW), a synchronized, terminal cell division that occurs several hours after passage of the furrow. We show that Combgap (Cg), a zinc-finger transcription factor, antagonizes Eya-So function in the SMW. Based on the ability of Cg to attenuate Eya-So transcriptional output in vivo and in cultured cells and on meta analysis of their chromatin occupancy profiles, we speculate that Cg limits Eya-So activation of select target genes posterior to the furrow to ensure properly timed mitotic exit. Our work supports a model in which context-specific modulation of transcriptional activity enables Eya and So to promote both entry into and exit from the cell cycle in a distinct spatiotemporal sequence.
PubMed ID
PubMed Central ID
PMC5536924 (PMC) (EuropePMC)
Related Publication(s)
Research paper

Pleiotropy in Drosophila organogenesis: Mechanistic insights from Combgap and the retinal determination gene network.
Davis and Rebay, 2018, Fly 12(1): 62--70 [FBrf0238707]

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Secondary IDs
    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 (1)
    Alleles (14)
    Genes (9)
    Physical Interactions (4)
    Cell Lines (1)
    Natural transposons (1)
    Experimental Tools (3)
    Transgenic Constructs (8)