scholarly journals Control of chromosome stability by the β-TrCP–REST–Mad2 axis

Nature ◽  
2008 ◽  
Vol 452 (7185) ◽  
pp. 365-369 ◽  
Author(s):  
Daniele Guardavaccaro ◽  
David Frescas ◽  
N. Valerio Dorrello ◽  
Angelo Peschiaroli ◽  
Asha S. Multani ◽  
...  
Keyword(s):  
Chromosome Stability

Chromosome Stability in Some Hexaploid Strains of Triticale 1

Crop Science ◽  
1969 ◽  
Vol 9 (2) ◽  
pp. 235-236 ◽  
Author(s):  
T. Tsuchiya ◽  
E. N. Larter
Keyword(s):  
Chromosome Stability

scholarly journals p53-dependent effects of RAS oncogene on chromosome stability and cell cycle checkpoints

Oncogene ◽  
1999 ◽  
Vol 18 (20) ◽  
pp. 3135-3142 ◽  
Author(s):  
LS Agapova ◽  
AV Ivanov ◽  
AA Sablina ◽  
PB Kopnin ◽  
OI Sokova ◽  
...  
Keyword(s):  
Cell Cycle ◽  
Cell Cycle Checkpoints ◽  
Chromosome Stability ◽  
Ras Oncogene

O191. Chromosome stability in tonsillar squamous cell carcinoma is associated with HPV and a favorable prognosis

2009 ◽  
Vol 3 (1) ◽  
pp. 119-120 ◽  
Author(s):  
J.J. Mooren ◽  
A.H.N. Hopman ◽  
F.C.S. Ramaekers ◽  
J.J. Manni ◽  
B. Kremer ◽  
...  
Keyword(s):  
Squamous Cell Carcinoma ◽  
Cell Carcinoma ◽  
Squamous Cell ◽  
Chromosome Stability ◽  
Favorable Prognosis ◽  
Tonsillar Squamous Cell Carcinoma

scholarly journals Both R-loop removal and ribonucleotide excision repair activities of RNase H2 contribute substantially to chromosome stability

DNA Repair ◽  
2017 ◽  
Vol 52 ◽  
pp. 110-114 ◽  
Author(s):  
Deborah A. Cornelio ◽  
Hailey N.C. Sedam ◽  
Jessica A. Ferrarezi ◽  
Nadia M.V. Sampaio ◽  
Juan Lucas Argueso
Keyword(s):  
Excision Repair ◽  
Chromosome Stability ◽  
Rnase H2

Effects of excess centromeres and excess telomeres on chromosome loss rates

1991 ◽  
Vol 11 (6) ◽  
pp. 2919-2928
Author(s):  
K W Runge ◽  
R J Wellinger ◽  
V A Zakian
Keyword(s):  
Saccharomyces Cerevisiae ◽  
Cell Division ◽  
Dna Sequences ◽  
Fluctuation Analysis ◽  
Chromosome Stability ◽  
Chromosome Loss ◽  
Division Iii ◽  
Daughter Cells ◽  
Chromosome Iii ◽  
Linear Chromosomes

The linear chromosomes of eukaryotes contain specialized structures to ensure their faithful replication and segregation to daughter cells. Two of these structures, centromeres and telomeres, are limited, respectively, to one and two copies per chromosome. It is possible that the proteins that interact with centromere and telomere DNA sequences are present in limiting amounts and could be competed away from the chromosomal copies of these elements by additional copies introduced on plasmids. We have introduced excess centromeres and telomeres into Saccharomyces cerevisiae and quantitated their effects on the rates of loss of chromosome III and chromosome VII by fluctuation analysis. We show that (i) 600 new telomeres have no effect on chromosome loss; (ii) an average of 25 extra centromere DNA sequences increase the rate of chromosome III loss from 0.4 x 10(-4) events per cell division to 1.3 x 10(-3) events per cell division; (iii) centromere DNA (CEN) sequences on circular vectors destabilize chromosomes more effectively than do CEN sequences on 15-kb linear vectors, and transcribed CEN sequences have no effect on chromosome stability. We discuss the different effects of extra centromere and telomere DNA sequences on chromosome stability in terms of how the cell recognizes these two chromosomal structures.

The effect on chromosome stability of deleting replication origins

1993 ◽  
Vol 13 (1) ◽  
pp. 391-398
Author(s):  
A Dershowitz ◽  
C S Newlon
Keyword(s):  
Ring Chromosome ◽  
High Rate ◽  
Chromosome Stability ◽  
Replication Origins ◽  
Chromosomal Dna ◽  
Circular Chromosome ◽  
Cell Cycles ◽  
Highly Active ◽  
Dna Replication Origins ◽  
Chromosome Iii

The observed spacing between chromosomal DNA replication origins in Saccharomyces cerevisiae is at least four times shorter than should be necessary to ensure complete replication of chromosomal DNA during the S phase. To test whether all replication origins are required for normal chromosome stability, the loss rates of derivatives of chromosome III from which one or more origins had been deleted were measured. In the case of a 61-kb circular derivative of the chromosome that has two highly active origins and one origin that initiates only 10 to 20% of the time, deletion of either highly active origin increased its rate of loss two- to fourfold. Deletion of both highly active origins caused the ring chromosome to be lost in approximately 20% of cell divisions. This very high rate of loss demonstrates that there are no efficient cryptic origins on the ring chromosome that are capable of ensuring its replication in the absence of the origins that are normally used. Deletion of the same two origins from the full-length chromosome III, which contains more than six replication origins, had no effect on its rate of loss. These results suggest that the increase in the rate of loss of the small circular chromosome from which a single highly active origin was deleted was caused by the failure of the remaining highly active origin to initiate replication in a small fraction (approximately 0.003) of cell cycles.

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