GSBS Student Publications


DNA-replication checkpoint control at the Drosophila midblastula transition

UMMS Affiliation

Graduate School of Biomedical Sciences; Program in Molecular Medicine



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Medical Subject Headings

Animals; Blastocyst; Cell Cycle; Cyclin-Dependent Kinases; *DNA Replication; *Drosophila Proteins; Drosophila melanogaster; Female; Genes, Insect; Genetic Complementation Test; Male; Mitosis; Mitotic Spindle Apparatus; Mutation; Phosphoprotein Phosphatases; Phosphorylation; *Protein Tyrosine Phosphatases; Protein-Serine-Threonine Kinases; Transcription, Genetic


Life Sciences | Medicine and Health Sciences


Embryogenesis is typically initiated by a series of rapid mitotic divisions that are under maternal genetic control. The switch to zygotic control of embryogenesis at the midblastula transition is accompanied by significant increases in cell-cycle length and gene transcription, and changes in embryo morphology. Here we show that mutations in the grapes (grp) checkpoint 1 kinase homologue in Drosophila block the morphological and biochemical changes that accompany the midblastula transition, lead to a continuation of the maternal cell-cycle programme, and disrupt DNA-replication checkpoint control of cell-cycle progression. The timing of the midblastula transition is controlled by the ratio of nuclei to cytoplasm (the nucleocytoplasmic ratio), suggesting that this developmental transition is triggered by titration of a maternal factor by the increasing mass of nuclear material that accumulates during the rapid embryonic mitoses. Our observations support a model for cell-cycle control at the midblastula transition in which titration of a maternal component of the DNA-replication machinery slows DNA synthesis and induces a checkpoint-dependent delay in cell-cycle progression. This delay may allow both completion of S phase and transcription of genes that initiate the switch to zygotic control of embryogenesis.

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Citation: Nature. 1997 Jul 3;388(6637):93-7. Link to article on publisher's site

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