DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos

• Published in: Nature cell biology Vol. 2; no. 2; pp. 90 - 95
• Main Authors: Sibon, Ody C. M., Kelkar, Anju, Lemstra, Willy, Theurkauf, William E.
• Format: Journal Article
• Language: English
• Published: London Nature Publishing Group UK 01.02.2000; Nature Publishing Group
• Subjects: Animals; Aphidicolin - pharmacology; Biomedical and Life Sciences; Cancer Research; Cell Biology; Cell cycle; Centrosome - physiology; Centrosomes; Chromosome Aberrations; Chromosomes; Control systems; Deoxyribonucleic acid; Developmental Biology; DNA; DNA Damage; DNA Replication; Drosophila; Drosophila - embryology; Drosophila - genetics; Drosophila melanogaster; Embryonic growth stage; Embryos; Genetic aspects; Inactivation; Insects; Kinases; Life Sciences; Localization; Mitosis - genetics; Mutagens - pharmacology; Mutation; Physiological aspects; Spindle Apparatus - pathology; Stem Cells; Tubulin
• ISSN: 1465-7392; 1476-4679; 1476-4679
• DOI: 10.1038/35000041

During early embryogenesis of Drosophila melanogaster , mutations in the DNA-replication checkpoint lead to chromosome-segregation failures. Here we show that these segregation failures are associated with the assembly of an anastral microtubule spindle, a mitosis-specific loss of centrosome function, and dissociation of several components of the γ-tubulin ring complex from a core centrosomal structure. The DNA-replication inhibitor aphidicolin and DNA-damaging agents trigger identical mitotic defects in wild-type embryos, indicating that centrosome inactivation is a checkpoint-independent and mitosis-specific response to damaged or incompletely replicated DNA. We propose that centrosome inactivation is part of a damage-control system that blocks chromosome segregation when replication/damage checkpoint control fails.