scholarly journals Repair of DNA interstrand cross-links during S phase of the mammalian cell cycle

2010 ◽  
pp. NA-NA ◽  
Author(s):  
Randy J. Legerski
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
S Phase ◽  
Mammalian Cell Cycle ◽  
Interstrand Cross Links ◽  
Cross Links

Prediction of Key Factor Controlling G1/S Phase in the Mammalian Cell Cycle Using System Analysis

2008 ◽  
Vol 106 (4) ◽  
pp. 368-374 ◽  
Author(s):  
Yoshihiko Tashima ◽  
Hiroyuki Hamada ◽  
Masahiro Okamoto ◽  
Taizo Hanai
Keyword(s):  
Cell Cycle ◽  
Mammalian Cell ◽  
System Analysis ◽  
S Phase ◽  
Mammalian Cell Cycle ◽  
Key Factor

scholarly journals Restriction Point timing and cell cycle variability – a re-evaluation

2020 ◽  
Author(s):  
Robert F. Brooks
Keyword(s):  
Cell Cycle ◽  
Growth Factor ◽  
Mammalian Cell ◽  
Time Lapse ◽  
S Phase ◽  
Critical Transition ◽  
Restriction Point ◽  
Cycle Times ◽  
Mammalian Cell Cycle ◽  
Step Down

AbstractThe Restriction Point (R) in the mammalian cell cycle is regarded as a critical transition in G1 when cells become committed to enter S phase even in the absence of further growth factor stimulation. Classic time-lapse studies by Zetterberg and Larsson suggested that the acquisition of growth factor independence (i.e. passage of R) occurred very abruptly 3-4 hours after mitosis, with most cell cycle variability arising between R and entry into S phase. However, the cycle times of the post-R cells that continued on to mitosis after serum step-down without perturbation were far less variable than the control cells with which they were compared. A re-analysis of the data, presented here, shows that when the timing of R and entry in mitosis are compared for the same experiments, the curves are superimposable and statistically indistinguishable. This indicates that the data are compatible with the timing of R contributing to much of the overall variability in the cell cycle, contrary to the conclusions of Zetterberg and colleagues.

scholarly journals Towards a systems biology approach to mammalian cell cycle: modeling the entrance into S phase of quiescent fibroblasts after serum stimulation

2009 ◽  
Vol 10 (Suppl 12) ◽  
pp. S16 ◽  
Author(s):  
Roberta Alfieri ◽  
Matteo Barberis ◽  
Ferdinando Chiaradonna ◽  
Daniela Gaglio ◽  
Luciano Milanesi ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Systems Biology ◽  
Mammalian Cell ◽  
S Phase ◽  
Serum Stimulation ◽  
Mammalian Cell Cycle

Complementation of G1-phase variants of a mammalian cell cycle

1979 ◽  
Vol 35 (1) ◽  
pp. 53-58
Author(s):  
P.M. Naha
Keyword(s):  
Cell Cycle ◽  
Cell Fusion ◽  
Mammalian Cell ◽  
S Phase ◽  
G1 Phase ◽  
Temperature Sensitive ◽  
Multinucleated Cells ◽  
Mammalian Cell Cycle ◽  
Complementation Groups ◽  
Phase Variants

Complementation between temperature-sensitive (ts) variants of Balb/c-3T3 defective in the G1 phase of its cell cycle was measured in the [3H]thymidine-labeling indices of the multinucleated cells during incubation at the restricted temperature (38 degrees C) following cell fusion. One ts variant from each group along the length of the G1 phase was tested for complementation. Varying degrees of complementation were observed between the 4 ts variants tested, judging by the time of entry into S-phase and the degree of synchrony attained. At least 3 complementation groups were discernible.

scholarly journals DNA Interstrand Cross-Link Repair in the Saccharomyces cerevisiae Cell Cycle: Overlapping Roles for PSO2 (SNM1) with MutS Factors and EXO1 during S Phase

2005 ◽  
Vol 25 (6) ◽  
pp. 2297-2309 ◽  
Author(s):  
Louise J. Barber ◽  
Thomas A. Ward ◽  
John A. Hartley ◽  
Peter J. McHugh
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Cycle ◽  
Homologous Recombination ◽  
S Phase ◽  
Cycle Phase ◽  
Dna Double Strand Breaks ◽  
Recombination Rates ◽  
Strand Breaks ◽  
Interstrand Cross Links ◽  
Cross Links

ABSTRACT Pso2/Snm1 is a member of the β-CASP metallo-β-lactamase family of proteins that include the V(D)J recombination factor Artemis. Saccharomyces cerevisiae pso2 mutants are specifically sensitive to agents that induce DNA interstrand cross-links (ICLs). Here we establish a novel overlapping function for PSO2 with MutS mismatch repair factors and the 5′-3′ exonuclease Exo1 in the repair of DNA ICLs, which is confined to S phase. Our data demonstrate a requirement for NER and Pso2, or Exo1 and MutS factors, in the processing of ICLs, and this is required prior to the repair of ICL-induced DNA double-strand breaks (DSBs) that form during replication. Using a chromosomally integrated inverted-repeat substrate, we also show that loss of both pso2 and exo1/msh2 reduces spontaneous homologous recombination rates. Therefore, PSO2, EXO1, and MSH2 also appear to have overlapping roles in the processing of some forms of endogenous DNA damage that occur at an irreversibly collapsed replication fork. Significantly, our analysis of ICL repair in cells synchronized for each cell cycle phase has revealed that homologous recombination does not play a major role in the direct repair of ICLs, even in G2, when a suitable template is readily available. Rather, we propose that recombination is primarily involved in the repair of DSBs that arise from the collapse of replication forks at ICLs. These findings have led to considerable clarification of the complex genetic relationship between various ICL repair pathways.

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