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 inNature 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
LanguageEnglish
Published London Nature Publishing Group UK 01.02.2000
Nature Publishing Group
Subjects
Online AccessGet full text
ISSN1465-7392
1476-4679
1476-4679
DOI10.1038/35000041

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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.
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
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  givenname: Anju
  surname: Kelkar
  fullname: Kelkar, Anju
  organization: Program in Molecular Medicine and Department of Molecular Genetics and Microbiology, University of Massachusetts Medical Center
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  givenname: Willy
  surname: Lemstra
  fullname: Lemstra, Willy
  organization: Department of Radiobiology, Faculty of Medicine, University of Groningen
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  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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PublicationDateYYYYMMDD 2000-02-01
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  year: 2000
  text: 2000-02-01
  day: 01
PublicationDecade 2000
PublicationPlace London
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PublicationTitle Nature cell biology
PublicationTitleAbbrev Nat Cell Biol
PublicationTitleAlternate Nat Cell Biol
PublicationYear 2000
Publisher Nature Publishing Group UK
Nature Publishing Group
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10655600 - Nat Cell Biol. 2000 Feb;2(2):E28-9
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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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StartPage 90
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
URI https://link.springer.com/article/10.1038/35000041
https://www.ncbi.nlm.nih.gov/pubmed/10655588
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https://www.proquest.com/docview/759319072
Volume 2
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