Chk1 and Wee1 kinases coordinate DNA replication, chromosome condensation, and anaphase entry

Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, usin...

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Published inMolecular biology of the cell Vol. 23; no. 6; pp. 1047 - 1057
Main Authors Fasulo, Barbara, Koyama, Carol, Yu, Kristina R., Homola, Ellen M., Hsieh, Tao S., Campbell, Shelagh D., Sullivan, William
Format Journal Article
LanguageEnglish
Published United States The American Society for Cell Biology 15.03.2012
Subjects
Anaphase
Animals
Antitumor agents
Aphidicolin
Camptothecin
Cancer
Cell cycle
Cell Cycle Proteins - metabolism
Checkpoint Kinase 1
CHK1 protein
Chromosomes
Chromosomes - metabolism
Cisplatin
Condensation
DNA biosynthesis
DNA Replication
Doxorubicin
Drosophila
Drosophila melanogaster - cytology
Drosophila melanogaster - embryology
Embryos
Hydroxyurea
Ionizing radiation
Mechlorethamine
Metaphase
Nuclear Envelope - metabolism
Nuclear Proteins - metabolism
Protein Kinases - metabolism
Protein-Tyrosine Kinases - metabolism
Replication
S Phase
Spindles
Topoisomerase Inhibitors - pharmacology
Online AccessGet full text
ISSN1059-1524
1939-4586
1939-4586
DOI10.1091/mbc.e11-10-0832

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Abstract Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, using the rapid division cycles in the early Drosophila embryo. We find that S-phase and topoisomerase inhibitors delay both the initiation and the rate of chromosome condensation. These cell cycle delays are mediated by the cell cycle kinases chk1 and wee1. Inhibitors that cause severe defects in chromosome condensation and congression on the metaphase plate result in delayed anaphase entry. These delays are mediated by wee1 and are not the result of spindle assembly checkpoint activation. In addition, we provide the first detailed live analysis of the direct effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasmic cell cycle events.
AbstractList Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, using the rapid division cycles in the early Drosophila embryo. We find that S-phase and topoisomerase inhibitors delay both the initiation and the rate of chromosome condensation. These cell cycle delays are mediated by the cell cycle kinases chk1 and wee1. Inhibitors that cause severe defects in chromosome condensation and congression on the metaphase plate result in delayed anaphase entry. These delays are mediated by wee1 and are not the result of spindle assembly checkpoint activation. In addition, we provide the first detailed live analysis of the direct effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasmic cell cycle events.Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, using the rapid division cycles in the early Drosophila embryo. We find that S-phase and topoisomerase inhibitors delay both the initiation and the rate of chromosome condensation. These cell cycle delays are mediated by the cell cycle kinases chk1 and wee1. Inhibitors that cause severe defects in chromosome condensation and congression on the metaphase plate result in delayed anaphase entry. These delays are mediated by wee1 and are not the result of spindle assembly checkpoint activation. In addition, we provide the first detailed live analysis of the direct effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasmic cell cycle events.
Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, using the rapid division cycles in the early Drosophila embryo. We find that S-phase and topoisomerase inhibitors delay both the initiation and the rate of chromosome condensation. These cell cycle delays are mediated by the cell cycle kinases chk1 and wee1. Inhibitors that cause severe defects in chromosome condensation and congression on the metaphase plate result in delayed anaphase entry. These delays are mediated by wee1 and are not the result of spindle assembly checkpoint activation. In addition, we provide the first detailed live analysis of the direct effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasmic cell cycle events.
New chromosome condensation checkpoints are identified. S-phase and topoisomerase inhibitors delay chromosome condensation. These delays require chk1 and wee1 . Inhibitors causing defects in chromosome condensation/congression on the metaphase plate delay anaphase entry. wee1 and not the spindle assembly checkpoint mediates the delay. Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established, but little is known about the role of checkpoints in monitoring chromosome condensation. We investigate this function by live analysis, using the rapid division cycles in the early Drosophila embryo. We find that S-phase and topoisomerase inhibitors delay both the initiation and the rate of chromosome condensation. These cell cycle delays are mediated by the cell cycle kinases chk1 and wee1 . Inhibitors that cause severe defects in chromosome condensation and congression on the metaphase plate result in delayed anaphase entry. These delays are mediated by wee1 and are not the result of spindle assembly checkpoint activation. In addition, we provide the first detailed live analysis of the direct effect of widely used anticancer agents (aclarubicin, ICRF-193, VM26, doxorubicin, camptothecin, aphidicolin, hydroxyurea, cisplatin, mechlorethamine and x-rays) on key nuclear and cytoplasmic cell cycle events.
Author Campbell, Shelagh D.
Yu, Kristina R.
Hsieh, Tao S.
Fasulo, Barbara
Koyama, Carol
Homola, Ellen M.
Sullivan, William
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Snippet Defects in DNA replication and chromosome condensation are common phenotypes in cancer cells. A link between replication and condensation has been established,...
New chromosome condensation checkpoints are identified. S-phase and topoisomerase inhibitors delay chromosome condensation. These delays require chk1 and wee1...
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StartPage 1047
SubjectTerms Anaphase
Animals
Antitumor agents
Aphidicolin
Camptothecin
Cancer
Cell cycle
Cell Cycle Proteins - metabolism
Checkpoint Kinase 1
CHK1 protein
Chromosomes
Chromosomes - metabolism
Cisplatin
Condensation
DNA biosynthesis
DNA Replication
Doxorubicin
Drosophila
Drosophila melanogaster - cytology
Drosophila melanogaster - embryology
Embryos
Hydroxyurea
Ionizing radiation
Mechlorethamine
Metaphase
Nuclear Envelope - metabolism
Nuclear Proteins - metabolism
Protein Kinases - metabolism
Protein-Tyrosine Kinases - metabolism
Replication
S Phase
Spindles
Topoisomerase Inhibitors - pharmacology
Title Chk1 and Wee1 kinases coordinate DNA replication, chromosome condensation, and anaphase entry
URI https://www.ncbi.nlm.nih.gov/pubmed/22262459
https://www.proquest.com/docview/1008831743
https://www.proquest.com/docview/928373398
https://pubmed.ncbi.nlm.nih.gov/PMC3302732
Volume 23
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