DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos
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 functio...
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Published in | Nature cell biology Vol. 2; no. 2; pp. 90 - 95 |
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Main Authors | , , , |
Format | Journal Article |
Language | English |
Published |
London
Nature Publishing Group UK
01.02.2000
Nature Publishing Group |
Subjects | |
Online Access | Get full text |
ISSN | 1465-7392 1476-4679 1476-4679 |
DOI | 10.1038/35000041 |
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Abstract | 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. |
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AbstractList | 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. 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 gamma-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. 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 gamma-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.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 gamma-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. 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 g-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. |
Audience | Academic |
Author | Sibon, Ody C. M. Lemstra, Willy Kelkar, Anju Theurkauf, William E. |
Author_xml | – sequence: 1 givenname: Ody C. M. surname: Sibon fullname: Sibon, Ody C. M. organization: Department of Radiobiology, Faculty of Medicine, University of Groningen – sequence: 2 givenname: Anju surname: Kelkar fullname: Kelkar, Anju organization: Program in Molecular Medicine and Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center – sequence: 3 givenname: Willy surname: Lemstra fullname: Lemstra, Willy organization: Department of Radiobiology, Faculty of Medicine, University of Groningen – sequence: 4 givenname: William E. surname: Theurkauf fullname: Theurkauf, William E. email: william.theurkauf@umassmed.edu organization: Program in Molecular Medicine and Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center |
BackLink | https://www.ncbi.nlm.nih.gov/pubmed/10655588$$D View this record in MEDLINE/PubMed |
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Snippet | During early embryogenesis of
Drosophila melanogaster
, mutations in the DNA-replication checkpoint lead to chromosome-segregation failures. Here we show that... During early embryogenesis of Drosophila melanogaster, mutations in the DNA-replication checkpoint lead to chromosome-segregation failures. Here we show that... |
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SubjectTerms | 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 |
Title | DNA-replication/DNA-damage-dependent centrosome inactivation in Drosophila embryos |
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