Jove
Visualize
Contact Us
JoVE
x logofacebook logolinkedin logoyoutube logo
ABOUT JoVE
OverviewLeadershipBlogJoVE Help Center
AUTHORS
Publishing ProcessEditorial BoardScope & PoliciesPeer ReviewFAQSubmit
LIBRARIANS
TestimonialsSubscriptionsAccessResourcesLibrary Advisory BoardFAQ
RESEARCH
JoVE JournalMethods CollectionsJoVE Encyclopedia of ExperimentsArchive
EDUCATION
JoVE CoreJoVE BusinessJoVE Science EducationJoVE Lab ManualFaculty Resource CenterFaculty Site
Terms & Conditions of Use
Privacy Policy
Policies

Related Experiment Videos

Remodelling the Rad9 checkpoint complex: preparing Rad53 for action.

Michael van den Bosch1, Noel F Lowndes

  • 1Department of Biochemistry and National Centre for Biomedical Engineering Science, National University of Ireland Galway, Galway, Ireland.

Cell Cycle (Georgetown, Tex.)
|January 9, 2004
PubMed
Summary
This summary is machine-generated.

Related Concept Videos

You might also read

Related Articles

Articles linked to this work by shared authors, journal, and citation graph.

Sort by
Same author

Correction: Regulation of the DNA Damage Response and Gene Expression by the Dot1L Histone Methyltransferase and the 53Bp1 Tumour Suppressor.

PloS one·2024
Same author

DDX17 is required for efficient DSB repair at DNA:RNA hybrid deficient loci.

Nucleic acids research·2022
Same author

A function for ataxia telangiectasia and Rad3-related (ATR) kinase in cytokinetic abscission.

iScience·2022
Same author

Immediate-Early, Early, and Late Responses to DNA Double Stranded Breaks.

Frontiers in genetics·2022
Same author

Novel Pt(IV) Prodrugs Displaying Antimitochondrial Effects.

Molecular pharmaceutics·2020
Same author

Analysis of novel missense ATR mutations reveals new splicing defects underlying Seckel syndrome.

Human mutation·2018

The Rad9 protein forms distinct complexes that regulate DNA damage checkpoints. Chaperone activity remodels a large Rad9 complex into a smaller one, activating the Rad53 kinase to maintain genomic integrity.

Area of Science:

  • Cellular Biology
  • Molecular Biology
  • Genetics

Background:

  • DNA damage checkpoints are crucial for maintaining genomic stability after genotoxic stress.
  • Rad9 protein is essential for the Mec1-dependent activation of Rad53 in Saccharomyces cerevisiae DNA damage response.

Purpose of the Study:

  • To elucidate the structural dynamics of Rad9 complexes in response to DNA damage.
  • To propose a model for Rad9 complex remodeling and Rad53 activation.

Main Methods:

  • Purification of distinct Rad9 complexes.
  • Biochemical characterization of protein complexes.
  • Analysis of complex formation under different cellular conditions.

Main Results:

Related Experiment Videos

  • Two distinct Rad9 complexes were purified: a large 850 kDa complex (hypophosphorylated Rad9, Ssa1/2) and a smaller 560 kDa complex (hyperphosphorylated Rad9, Ssa1/2, Rad53).
  • The large complex is present in both undamaged and damaged cells, while the smaller complex forms only upon DNA damage.
  • Rad53 is activated by in trans autophosphorylation within the smaller complex.

    • Conclusions:

    • A model is proposed where chaperone activity remodels the large Rad9 complex into the smaller, Rad53-activating complex after genomic insult.
    • This remodeling is a key step in the DNA damage checkpoint pathway for effector kinase activation.