Cited by 147DNA Repair MechanismsFungal and yeast genetics researchBacterial Genetics and Biotechnology

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RAD9 and RAD24 define two additive, interacting branches of the DNA damage checkpoint pathway in budding yeast normally required for Rad53 modification and activation

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de la Torre‐Ruiz, Maria‐Angeles, Green, Catherine M., Lowndes, Noel F.·1998·The EMBO Journal

DOI 10.1093/emboj/17.9.2687PMC PMC1170609

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Abstract

In budding yeast, RAD9 and RAD24/RAD17/MEC3 are believed to function upstream of MEC1 and RAD53 in signalling the presence of DNA damage. Deletion of any one of these genes reduces the normal G1/S and G2/M checkpoint delays after UV irradiation, whereas in rad9Delta-rad24Delta cells the G1/S checkpoint is undetectable, although there is a residual G2/M checkpoint. We have shown previously that RAD9 also controls the transcriptional induction of a DNA damage regulon (DDR). We now report that efficient DDR induction requires all the above-mentioned checkpoint genes. Residual induction of the DDR after UV irradiation observed in all single mutants is not detectable in rad9Delta-rad24Delta. We have examined the G2/M checkpoint and UV sensitivity of single mutants after overexpression of the checkpoint proteins. This analysis indicates that RAD9 and the RAD24 epistasis group can be placed onto two separate, additive branches that converge on MEC1 and RAD53. Furthermore, MEC3 appears to function downstream of RAD24/RAD17. The transcriptional response to DNA damage revealed unexpected and specific antagonism between RAD9 and RAD24. Further support for genetic interaction between RAD9 and RAD24 comes from study of the modification and activation of Rad53 after damage. Evidence for bypass of RAD53 function under some conditions is also presented.

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Authors: de la Torre‐Ruiz, M., Green, C. M., & Lowndes, N. F.
Corresponding author: Lowndes, Noel F.
ORCID: Lowndes, Noel F.
Venue: The EMBO Journal
Publisher: Springer Science and Business Media LLC
Published: 1998-05-01
Volume: 17
Issue: 9
Pages: 2687-2698
ISSN: 0261-4189 (ISSN-L)
1460-2075
DOI: 10.1093/emboj/17.9.2687
PMC: PMC1170609
OpenAlex: W2110112613
Cited by: 147
References: 33
Citations by year: 2024: 5 · 2023: 1 · 2021: 1 · 2020: 2 · 2019: 1 · 2017: 1 · 2016: 1 · 2015: 1 · 2014: 2 · 2013: 3 · 2012: 2
FWCI: 6.06
Type: journal article
Language: en
Open access: green
www.ncbi.nlm.nih.gov
Licence: www.springer.com/tdm (tdm)
www.springer.com/tdm (vor)
Locations: The EMBO Journal (publishedVersion)
Europe PMC (PubMed Central) (publishedVersion)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Topics: Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › DNA Repair Mechanisms
Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Fungal and yeast genetics research
Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Bacterial Genetics and Biotechnology
Keywords: Rad9, Rad24, Rad17, Mec1, Rad53, DNA damage checkpoint, G1/S checkpoint, G2/M checkpoint, DNA damage response, UV irradiation, epistasis, genetic interactions, Saccharomyces cerevisiae
MeSH terms: Mating Factor, Cell Cycle, DNA Damage, DNA-Binding Proteins, DNA, Fungal, Exodeoxyribonucleases, Fungal Proteins, Kinetics, Mitosis, Nuclear Proteins, Peptides, Phosphorylation, Saccharomyces cerevisiae, Ultraviolet Rays, Nocodazole, G1 Phase, G2 Phase, S Phase, Cell Cycle Proteins, Saccharomyces cerevisiae Proteins, Intracellular Signaling Peptides and Proteins

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RAD9 and RAD24 define two additive, interacting branches of the DNA damage checkpoint pathway in budding yeast normally required for Rad53 modification and activation

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