Bedoukian   RussellIPM   RussellIPM   Piezoelectric Micro-Sprayer


Home
Animal Taxa
Plant Taxa
Semiochemicals
Floral Compounds
Semiochemical Detail
Semiochemicals & Taxa
Synthesis
Control
Invasive spp.
References

Abstract

Guide

Alphascents
Pherobio
InsectScience
E-Econex
Counterpart-Semiochemicals
Print
Email to a Friend
Kindly Donate for The Pherobase

« Previous AbstractTesting the single-pass VOC removal efficiency of an active green wall using methyl ethyl ketone (MEK)    Next AbstractStructural basis for divergent and convergent evolution of catalytic machineries in plant aromatic amino acid decarboxylase proteins »

EMBO J


Title:"RAD9 and RAD24 define two additive, interacting branches of the DNA damage checkpoint pathway in budding yeast normally required for Rad53 modification and activation"
Author(s):Torre-Ruiz MA; Green CM; Lowndes NF;
Address:"Imperial Cancer Research Fund, Clare Hall Laboratories, CDC Laboratory, South Mimms, Herts EN6 3LD, UK"
Journal Title:EMBO J
Year:1998
Volume:17
Issue:9
Page Number:2687 - 2698
DOI: 10.1093/emboj/17.9.2687
ISSN/ISBN:0261-4189 (Print) 1460-2075 (Electronic) 0261-4189 (Linking)
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"
Keywords:"Cell Cycle/drug effects/*physiology/radiation effects Cell Cycle Proteins/*metabolism *DNA Damage DNA, Fungal/biosynthesis/drug effects/radiation effects DNA-Binding Proteins Exodeoxyribonucleases/metabolism Fungal Proteins/*metabolism G1 Phase G2 Phase I;"
Notes:"Medlinede la Torre-Ruiz, M A Green, C M Lowndes, N F eng Research Support, Non-U.S. Gov't England 1998/06/20 EMBO J. 1998 May 1; 17(9):2687-98. doi: 10.1093/emboj/17.9.2687"

 
Back to top
 
Citation: El-Sayed AM 2024. The Pherobase: Database of Pheromones and Semiochemicals. <http://www.pherobase.com>.
© 2003-2024 The Pherobase - Extensive Database of Pheromones and Semiochemicals. Ashraf M. El-Sayed.
Page created on 27-09-2024